Expression of glial fibrillary acidic protein in areas of focal cerebral ischemia accompanies neuronal expression of 72-kDa heat shock protein

Li, Yang; Chopp, Michael; Zhang, Zheng G.; Zhang, Rui L.

doi:10.1016/0022-510x(94)00228-g

Cited by 65 publications

(35 citation statements)

References 39 publications

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“…The activation of astrocytes, characterized by hyperplasia and hypertrophy, with increased GFAP immunoreactivity, has been reported following cerebral ischemia in the rats, [52][53][54] whereas other studies have reported an early decline of GFAP reactivity in the region of infarct following severe ischemic insults. 51,[55][56][57][58] To specifically investigate the temporal effects of pMCAO on astrocyte function, we measured the expression of GFAP at various time points following ischemic insult by immunohistochemistry. The present results revealed that compared with the GFAP staining in sham-operated cortex (Fig.…”

Section: Resultsmentioning

confidence: 99%

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Qin

Liu²,

Qin³

et al. 2010

Autophagy

188

160

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Section: Resultsmentioning

confidence: 99%

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Qin

Liu²,

Qin³

et al. 2010

Autophagy

188

160

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“…36,37 The osteopontin receptor integrin ␣ v ␤ 3 is expressed by astrocytes at 5 and 15 days after ischemia. These time points were chosen to identify potential cell populations that could interact with the osteopontin in the extracellular matrix.…”

Section: Discussionmentioning

confidence: 99%

Osteopontin and its Integrin Receptor α _v β ₃ Are Upregulated During Formation of the Glial Scar After Focal Stroke

Ellison¹,

Velier²,

Spera³

et al. 1998

Stroke

158

113

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Background and Purpose-Microglia and astrocytes in the peri-infarct region are activated in response to focal stroke. A critical function of activated glia is formation of a protective barrier that ultimately forms a new glial-limiting membrane. Osteopontin, a provisional matrix protein expressed during wound healing, is induced after focal stroke. The present study was performed to determine the spatial and temporal expression of osteopontin and its integrin receptor ␣ v ␤ 3 during formation of the peri-infarct gliotic barrier and subsequent formation of a new glial-limiting membrane. Methods-Spontaneously hypertensive rats (nϭ19) were subjected to permanent occlusion of the middle cerebral artery and killed 3, 6, and 24 hours and 2, 5, and 15 days after occlusion. The spatial and temporal expression of osteopontin mRNA was determined by in situ hybridization, and that of osteopontin ligand and its integrin receptor ␣ v ␤ 3 was determined by immunohistochemistry. Results-Osteopontin mRNA was expressed de novo in the peri-infarct region from 3 to 48 hours; by 5 days osteopontin mRNA expression was restricted to the infarct. Osteopontin protein was expressed by peri-infarct microglia beginning at 24 hours and by microglia/macrophages at 48 hours in the infarct. Integrin receptor ␣ v ␤ 3 was expressed in peri-infarct astrocytes at 5 and 15 days. Conclusions-Early

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“…The functional significance of such an astrocytic response surrounding focal cerebral infarcts is still unclear. 14,15 To further investigate the role of astrocyte response to ischemia, we took the advantage of GFAP-luc transgenic mice. 16 In this mouse model, the luciferase gene (firefly luciferase, luc) is driven by the GFAP promoter, and luciferase expression (bioluminescence photon emission) can be followed longitudinally in live animals by biophotonic imaging and a high-resolution CCD camera.…”

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confidence: 99%

Live Imaging of Neuroinflammation Reveals Sex and Estrogen Effects on Astrocyte Response to Ischemic Injury

Cordeau

Lalancette–Hébert

Weng

et al. 2008

Stroke

115

110

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Background and Purpose-We sought to develop a model system for live analysis of brain inflammatory response in ischemic injury. Methods-Using a reporter mouse-expressing luciferase gene under transcriptional control of the murine glial fibrillary acidic protein (GFAP) promoter (GFAP-luc mice) and biophotonic/bioluminescent imaging as tools, we developed a model system for in vivo analysis of astrocyte activation/response in cerebral ischemia. Results-Analysis of photon emissions from the brains of living animals revealed marked sex differences in astrocyte response to ischemic injury. The increase in GFAP signals was significantly higher in female mice in the metestrus/diestrus period compared with male transgenic mice (1.71ϫ10 7 Ϯ0.19ϫ10 7 vs 0.92ϫ10 7 Ϯ0.15ϫ10 7 , PϽ0.001). Similar results were obtained by quantitative immunohistochemistry (males vs females: 13.4Ϯ0.5 vs 16.96Ϯ0.64, PϽ0.0001). However, astrocyte activation/GFAP signals showed cyclic, estrus-dependent variations in response to ischemic injury. Physiologically higher levels of estrogen and application of pharmacologic doses of estrogen during replacement therapy attenuated GFAP upregulation after stroke. Interestingly, contrary to a positive correlation between the intensities of GFAP signals and infarct size in male mice, no such correlation was observed in any of the experimental groups of female GFAP-luc mice. Conclusions-Our results suggest that GFAP upregulation in ischemic injury may have different functional significance in female and male experimental animals and may not directly reflect the extent of ischemia-induced neuronal damage in female GFAP-luc mice. Using a novel live imaging approach, we demonstrated that the early-phase brain inflammatory response to ischemia may be associated with sex-specific biomarkers of brain damage.

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Expression of glial fibrillary acidic protein in areas of focal cerebral ischemia accompanies neuronal expression of 72-kDa heat shock protein

Cited by 65 publications

References 39 publications

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Osteopontin and its Integrin Receptor α _v β ₃ Are Upregulated During Formation of the Glial Scar After Focal Stroke

Live Imaging of Neuroinflammation Reveals Sex and Estrogen Effects on Astrocyte Response to Ischemic Injury

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Expression of glial fibrillary acidic protein in areas of focal cerebral ischemia accompanies neuronal expression of 72-kDa heat shock protein

Cited by 65 publications

References 39 publications

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Autophagy was activated in injured astrocytes and mildly decreased cell survival following glucose and oxygen deprivation and focal cerebral ischemia

Osteopontin and its Integrin Receptor α v β 3 Are Upregulated During Formation of the Glial Scar After Focal Stroke

Live Imaging of Neuroinflammation Reveals Sex and Estrogen Effects on Astrocyte Response to Ischemic Injury

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Osteopontin and its Integrin Receptor α _v β ₃ Are Upregulated During Formation of the Glial Scar After Focal Stroke