Source 1primary paper2012Asian Pacific Journal of Cancer Prevention
Toolkit/immunohistochemistry
immunohistochemistry
Also known as: IHC
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Immunohistochemistry is an antibody-based tissue staining assay used in the cited stroke study alongside transcriptomics and real-time polymerase chain reaction to examine post-stroke tissue in aged rats and post-stroke patients. In that context, it supported assessment of angiogenesis-related histological features such as vascular density after stroke.
Usefulness & Problems
Why this is useful
This assay is useful for visualizing tissue-associated biological features in situ using antibody staining. In the supplied evidence, it contributed histological assessment of post-stroke angiogenesis-related tissue changes when combined with molecular profiling approaches.
Problem solved
Immunohistochemistry helps address the problem of assessing tissue-level angiogenesis after stroke within intact specimens rather than relying only on transcript measurements. In the cited study context, it supported comparison of vascular density and related post-stroke tissue features between young and old rats and in post-stroke patient material.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete measurement method used to characterize an engineered system.
Target processes
No target processes tagged yet.
Input: Light
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationimplementation constraint: spectral hardware requirementmodality: tissue assaymodality: tissue stainingoperating role: sensorreview context: stress neurobiology
The available evidence indicates use of immunohistochemistry in combination with real-time polymerase chain reaction and stroke transcriptomics in aged rats and post-stroke patients. No further practical details are provided on fixation, antigen retrieval, detection chemistry, construct design, or required reagents beyond antibody-based tissue staining.
The supplied evidence does not specify the antibodies, antigens, staining protocol, quantification method, or imaging modality used for immunohistochemistry. It also does not provide performance metrics such as sensitivity, specificity, reproducibility, or independent benchmarking for this assay in the described application.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Source 2review2023Frontiers in Neuroscience
Source 3primary paper2023
Source 4review2019Annual Review of Neuroscience
Source 5primary paper2026MED
Source 6primary paper2014Frontiers in Aging Neuroscience
Ranked Claims
The reviewed literature uses chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry approaches to investigate the role of specific cell subtypes in the stress response.
many studies have used state-of-the-art tools such as chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry to investigate the role of specific cell subtypes in the stress response
Recent availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data has challenged the view that astrocytes are a homogeneous population across the CNS.
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.
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
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).
Approval Evidence
6 sources5 linked approval claimsfirst-pass slug immunohistochemistry
In situ hybridization (ISH) and immunohistochemistry (IHC) were performed to examine the pathway's effect on Smad4 expression in tendinopathic tenocytes and tendons.
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many studies have used state-of-the-art tools such as ... immunohistochemistry to investigate the role of specific cell subtypes in the stress response
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Using a combination of immunohistochemistry
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this view has been challenged in the last few years with the availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data
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by combining stroke transcriptomics with immunohistochemistry in aged rats and post-stroke patients
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Using real time polymerase chain reaction and immunohistochemistry techniques
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tool usage summarysupports
The reviewed literature uses chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry approaches to investigate the role of specific cell subtypes in the stress response.
many studies have used state-of-the-art tools such as chemogenetic, optogenetic, genetic manipulation, electrophysiology, pharmacology, and immunohistochemistry to investigate the role of specific cell subtypes in the stress response
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field summarysupports
Recent availability of RNA sequencing, immunohistochemistry, electron microscopy, morphological reconstruction, and imaging data has challenged the view that astrocytes are a homogeneous population across the CNS.
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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.
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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.
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human observationsupports
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
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Comparisons
Source-backed strengths
The evidence shows that immunohistochemistry was integrated with real-time polymerase chain reaction and stroke transcriptomics, indicating utility as a complementary tissue-level assay in multimodal studies. In the cited work, it supported biological observations about vigorous angiogenesis after stroke and age-associated differences in vascular density by day 14.
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Beyond this barrier, angiogenesis in the aged brains was similar to that in young brains.
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We found that both young and old infarcted rats initiated vigorous angiogenesis.
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However, the young rats had a higher vascular density by day 14 post-stroke.
Compared with Field-domain rapid-scan EPR at 240 GHz
immunohistochemistry and Field-domain rapid-scan EPR at 240 GHz address a similar problem space.
Shared frame: same top-level item type
Strengths here: appears more independently replicated; looks easier to implement in practice.
Compared with fluorescence line narrowing
immunohistochemistry and fluorescence line narrowing address a similar problem space.
Shared frame: same top-level item type
Strengths here: appears more independently replicated; looks easier to implement in practice.
Compared with native green gel system
immunohistochemistry and native green gel system address a similar problem space.
Shared frame: same top-level item type
Strengths here: appears more independently replicated; looks easier to implement in practice.
Ranked Citations
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