Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia

Daniel M. Rosenbaum, Gaurav Gupta, Jason D'Amore, Manjeet Singh, Karen M. Weidenheim, Hong Zhang, John A. Kessler

Research output: Contribution to journalArticle

129 Citations (Scopus)

Abstract

The purpose of this study was to investigate the role of fas antigen, a member of the TNF receptor family, in cell death after focal cerebral ischemia. Focal ischemia was induced in the Sprague-Dawley rat. Evidence for apoptosis was determined by morphology as well as the presence of DNA fragmentation by the end labeling technique (TUNEL). Immunohistochemistry was performed to detect expression of both fas and fas ligand (fasL). In a separate set of experiments, two groups of mice were studied: Ipr (that have a loss of function mutation for fas) and wild type. Infarct volume was measured at 24 hr as well as evidence for apoptosis. Twenty-four hours after ischemia, there was evidence for apoptosis based on morphological criteria as well as the TUNEL technique in the rat. Immunohistochemistry demonstrated increased expression of both fas and fasL in the ischemic region, with maximal staining occurring between 24-48 hr for both. Twenty-four hours after ischemia in the mice, there was evidence of apoptosis in both groups, however, the mutant mice (Ipr) had significantly smaller infarcts as compared to the wild type. There was no difference in the cerebrovasculature of the two groups of mice. These data support the hypothesis that apoptosis plays a role in the pathophysiology of focal cerebral ischemia. Furthermore, these data suggest that fas-mediated apoptosis contributes to this process. (C) 2000 Wiley-Liss, Inc.

Original languageEnglish (US)
Pages (from-to)686-692
Number of pages7
JournalJournal of Neuroscience Research
Volume61
Issue number6
DOIs
StatePublished - Sep 15 2000

Fingerprint

Brain Ischemia
Apoptosis
Fas Ligand Protein
Ischemia
In Situ Nick-End Labeling
Immunohistochemistry
CD95 Antigens
Tumor Necrosis Factor Receptors
DNA Fragmentation
Sprague Dawley Rats
Cell Death
Staining and Labeling
Mutation

Keywords

  • Apoptosis
  • Cerebral ischemia
  • Mice
  • Mutant
  • Rats

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia. / Rosenbaum, Daniel M.; Gupta, Gaurav; D'Amore, Jason; Singh, Manjeet; Weidenheim, Karen M.; Zhang, Hong; Kessler, John A.

In: Journal of Neuroscience Research, Vol. 61, No. 6, 15.09.2000, p. 686-692.

Research output: Contribution to journalArticle

Rosenbaum, Daniel M. ; Gupta, Gaurav ; D'Amore, Jason ; Singh, Manjeet ; Weidenheim, Karen M. ; Zhang, Hong ; Kessler, John A. / Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia. In: Journal of Neuroscience Research. 2000 ; Vol. 61, No. 6. pp. 686-692.
@article{c03f346fb3cc4756b22a36f177de58f5,
title = "Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia",
abstract = "The purpose of this study was to investigate the role of fas antigen, a member of the TNF receptor family, in cell death after focal cerebral ischemia. Focal ischemia was induced in the Sprague-Dawley rat. Evidence for apoptosis was determined by morphology as well as the presence of DNA fragmentation by the end labeling technique (TUNEL). Immunohistochemistry was performed to detect expression of both fas and fas ligand (fasL). In a separate set of experiments, two groups of mice were studied: Ipr (that have a loss of function mutation for fas) and wild type. Infarct volume was measured at 24 hr as well as evidence for apoptosis. Twenty-four hours after ischemia, there was evidence for apoptosis based on morphological criteria as well as the TUNEL technique in the rat. Immunohistochemistry demonstrated increased expression of both fas and fasL in the ischemic region, with maximal staining occurring between 24-48 hr for both. Twenty-four hours after ischemia in the mice, there was evidence of apoptosis in both groups, however, the mutant mice (Ipr) had significantly smaller infarcts as compared to the wild type. There was no difference in the cerebrovasculature of the two groups of mice. These data support the hypothesis that apoptosis plays a role in the pathophysiology of focal cerebral ischemia. Furthermore, these data suggest that fas-mediated apoptosis contributes to this process. (C) 2000 Wiley-Liss, Inc.",
keywords = "Apoptosis, Cerebral ischemia, Mice, Mutant, Rats",
author = "Rosenbaum, {Daniel M.} and Gaurav Gupta and Jason D'Amore and Manjeet Singh and Weidenheim, {Karen M.} and Hong Zhang and Kessler, {John A.}",
year = "2000",
month = "9",
day = "15",
doi = "10.1002/1097-4547(20000915)61:6<686::AID-JNR12>3.0.CO;2-7",
language = "English (US)",
volume = "61",
pages = "686--692",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "6",

}

TY - JOUR

T1 - Fas (CD95/APO-1) plays a role in the pathophysiology of focal cerebral ischemia

AU - Rosenbaum, Daniel M.

AU - Gupta, Gaurav

AU - D'Amore, Jason

AU - Singh, Manjeet

AU - Weidenheim, Karen M.

AU - Zhang, Hong

AU - Kessler, John A.

PY - 2000/9/15

Y1 - 2000/9/15

N2 - The purpose of this study was to investigate the role of fas antigen, a member of the TNF receptor family, in cell death after focal cerebral ischemia. Focal ischemia was induced in the Sprague-Dawley rat. Evidence for apoptosis was determined by morphology as well as the presence of DNA fragmentation by the end labeling technique (TUNEL). Immunohistochemistry was performed to detect expression of both fas and fas ligand (fasL). In a separate set of experiments, two groups of mice were studied: Ipr (that have a loss of function mutation for fas) and wild type. Infarct volume was measured at 24 hr as well as evidence for apoptosis. Twenty-four hours after ischemia, there was evidence for apoptosis based on morphological criteria as well as the TUNEL technique in the rat. Immunohistochemistry demonstrated increased expression of both fas and fasL in the ischemic region, with maximal staining occurring between 24-48 hr for both. Twenty-four hours after ischemia in the mice, there was evidence of apoptosis in both groups, however, the mutant mice (Ipr) had significantly smaller infarcts as compared to the wild type. There was no difference in the cerebrovasculature of the two groups of mice. These data support the hypothesis that apoptosis plays a role in the pathophysiology of focal cerebral ischemia. Furthermore, these data suggest that fas-mediated apoptosis contributes to this process. (C) 2000 Wiley-Liss, Inc.

AB - The purpose of this study was to investigate the role of fas antigen, a member of the TNF receptor family, in cell death after focal cerebral ischemia. Focal ischemia was induced in the Sprague-Dawley rat. Evidence for apoptosis was determined by morphology as well as the presence of DNA fragmentation by the end labeling technique (TUNEL). Immunohistochemistry was performed to detect expression of both fas and fas ligand (fasL). In a separate set of experiments, two groups of mice were studied: Ipr (that have a loss of function mutation for fas) and wild type. Infarct volume was measured at 24 hr as well as evidence for apoptosis. Twenty-four hours after ischemia, there was evidence for apoptosis based on morphological criteria as well as the TUNEL technique in the rat. Immunohistochemistry demonstrated increased expression of both fas and fasL in the ischemic region, with maximal staining occurring between 24-48 hr for both. Twenty-four hours after ischemia in the mice, there was evidence of apoptosis in both groups, however, the mutant mice (Ipr) had significantly smaller infarcts as compared to the wild type. There was no difference in the cerebrovasculature of the two groups of mice. These data support the hypothesis that apoptosis plays a role in the pathophysiology of focal cerebral ischemia. Furthermore, these data suggest that fas-mediated apoptosis contributes to this process. (C) 2000 Wiley-Liss, Inc.

KW - Apoptosis

KW - Cerebral ischemia

KW - Mice

KW - Mutant

KW - Rats

UR - http://www.scopus.com/inward/record.url?scp=0034666684&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034666684&partnerID=8YFLogxK

U2 - 10.1002/1097-4547(20000915)61:6<686::AID-JNR12>3.0.CO;2-7

DO - 10.1002/1097-4547(20000915)61:6<686::AID-JNR12>3.0.CO;2-7

M3 - Article

VL - 61

SP - 686

EP - 692

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 6

ER -