Source 1primary paper2014Frontiers in Aging Neuroscience
Toolkit/stroke transcriptomics
stroke transcriptomics
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Stroke transcriptomics is a gene-expression profiling assay applied to post-stroke tissue and combined with immunohistochemistry in aged rats and post-stroke patients. In the cited study, it was used to characterize post-stroke angiogenesis-associated transcriptional programs and relate them to vascular density differences across age groups.
Usefulness & Problems
Why this is useful
This assay method is useful for linking post-stroke transcriptional states to histological vascular phenotypes in injured brain tissue. The cited evidence indicates utility for comparing angiogenesis-related responses between young and aged brains and for integrating molecular profiling with immunohistochemical observations.
Problem solved
It addresses the problem of how to assess age-dependent molecular and tissue-level features of angiogenesis after stroke in the same experimental framework. In the cited work, it helped examine why vascular density differed by day 14 post-stroke despite vigorous angiogenesis in both young and old infarcted rats.
Problem links
Need conditional recombination or state switching
DerivedStroke transcriptomics is a gene-expression profiling assay applied to post-stroke tissue and combined with immunohistochemistry in aged rats and post-stroke patients. In the cited study, it was used to characterize angiogenesis-associated transcriptional programs after stroke and relate them to vascular density differences between young and aged brains.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete measurement method used to characterize an engineered system.
Mechanisms
correlative association of transcript abundance with vascular densitycorrelative association of transcript abundance with vascular densitygene expression profilinggene expression profilinghistology-integrated phenotypic validationhistology-integrated phenotypic validationTarget processes
recombinationImplementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: sensor
The available evidence indicates use on post-stroke tissue with combination of transcriptomics and immunohistochemistry in aged rats and post-stroke patients. No further practical details are provided here regarding RNA preparation, platform type, normalization, staining markers, or construct and delivery considerations.
The supplied evidence describes application to post-stroke angiogenesis but does not specify the transcriptomic platform, gene panel, sampling design, or analytical pipeline. Validation breadth is limited by the provided evidence, which centers on a single cited study and mainly comparative biological observations rather than assay performance metrics.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
time post stroke 14 day
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
The aged human brain is capable of mounting a vigorous angiogenic response after stroke.
We also found that the aged human brain is capable of mounting a vigorous angiogenic response after stroke
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
Approval Evidence
1 source6 linked approval claimsfirst-pass slug stroke-transcriptomics
by combining stroke transcriptomics with immunohistochemistry in aged rats and post-stroke patients
Source:
comparative biological observationsupports
Beyond the inflammatory and fibrotic barrier, angiogenesis in aged brains was similar to that in young brains.
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Source:
comparative biological observationsupports
Both young and old infarcted rats initiated vigorous angiogenesis after stroke.
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Source:
comparative biological observationsupports
Young rats had higher vascular density than old rats by day 14 post-stroke.
However, the young rats had a higher vascular density by day 14 post-stroke.
Source:
gene expression associationsupports
Genes including Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4 were linked to increased vasculature density in young animals and are required for sprouting angiogenesis, basal lamina reconstruction, and the resolution phase.
"New-for-stroke" genes that were linked to the increased vasculature density in young animals included Angpt2, Angptl2, Angptl4, Cib1, Ccr2, Col4a2, Cxcl1, Lef1, Hhex, Lamc1, Nid2, Pcam1, Plod2, Runx3, Scpep1, S100a4, Tgfbi, and Wnt4, which are required for sprouting angiogenesis, reconstruction of the basal lamina (BL), and the resolution phase.
Source:
gene expression timingsupports
Most genes involved in sprouting angiogenesis, basal lamina reconstruction, and tube formation or maturation showed delayed upregulation in aged rats.
The vast majority of genes involved in sprouting angiogenesis (Angpt2, Angptl4, Cib1, Col8a1, Nrp1, Pcam1, Pttg1ip, Rac2, Runx1, Tnp4, Wnt4); reconstruction of a new BL (Col4a2, Lamc1, Plod2); or tube formation and maturation (Angpt1, Gpc3, Igfbp7, Sparc, Tie2, Tnfsf10), had however, a delayed upregulation in the aged rats.
Source:
mechanistic interpretationsupports
In aged rats, persistent upregulation of inflammatory genes and strong expression of fibrotic scar genes further diminished the angiogenic response.
The angiogenic response in aged rats was further diminished by the persistent upregulation of "inflammatory" genes (Cxcl12, Mmp8, Mmp12, Mmp14, Mpeg1, Tnfrsf1a, Tnfrsf1b) and vigorous expression of genes required for the buildup of the fibrotic scar (Cthrc1, Il6ra, Il13ar1, Il18, Mmp2, Rassf4, Tgfb1, Tgfbr2, Timp1).
Source:
Comparisons
Source-backed strengths
A reported strength is integration of transcriptomics with immunohistochemistry, enabling molecular-histological comparison in aged rats and post-stroke patients. The study also reports biologically discriminative findings, including higher vascular density in young rats by day 14 post-stroke and broadly similar angiogenesis in aged brains beyond inflammatory and fibrotic barriers.
Source:
Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
Source:
We found that both young and old infarcted rats initiated vigorous angiogenesis.
Source:
However, the young rats had a higher vascular density by day 14 post-stroke.
Compared with chromatin in vivo imaging
stroke transcriptomics and chromatin in vivo imaging address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination
Compared with light-dark masking paradigm
stroke transcriptomics and light-dark masking paradigm address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination
Strengths here: looks easier to implement in practice.
Compared with whole genome screening of gene knockout mutants
stroke transcriptomics and whole genome screening of gene knockout mutants address a similar problem space because they share recombination.
Shared frame: same top-level item type; shared target processes: recombination
Ranked Citations
- 1.