Monitoring the temporal and spatial activation pattern of astrocytes in focal cerebral ischemia using in situ hybridization to GFAP mRNA: comparison withsgp-2 andhsp70 mRNA and the effect of glutamate receptor antagonists

Glial responses, clusterin, and complement in permanent focal cerebral ischemia in the mouse

“…Clusterin has complement inhibitory properties by complexing with C5b-7 but is also involved in a number of other functions, such as cell-cell interaction and lipid transport. Increased expression of clusterin has been described in several brain lesion models including cerebral ischemia (Llampert-Etchells et al, 1991;Pasinetti et al, 1991;May et al, 1992May et al, , 1996Yamashita et al, 1996). We observed an increased expression of clusterin mRNA in the ischemic cortex after MCA occlusion at 3 days after the onset of cerebral ischemia.…”

“…We observed an increased expression of clusterin mRNA in the ischemic cortex after MCA occlusion at 3 days after the onset of cerebral ischemia. Using in situ hybridization, we found an increased expression of clusterin mRNA in brain regions surrounding the ischemic core within days after the onset of focal cerebral ischemia as described before in the rat (Yamashita et al, 1996). Immunohistochemical experiments showed reactive astrocytes strongly stained for clusterin in the perifocal area.…”

“…Astroglial response to ischemic injury was assessed by evaluating GFAP upregulation at both the mRNA and protein levels. These progressive changes in GFAP mRNA (Yamashita et al, 1996) and protein (Clark et al, 1993) expression were documented earlier in a rat model of permanent focal ischemia. However, to our best knowledge, there was no available data concerning the astroglial response in this model of permanent focal cerebral ischemia in the mouse.…”

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

“…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.…”

11C-DPA-713: A Novel Peripheral Benzodiazepine Receptor PET Ligand for In Vivo Imaging of Neuroinflammation

“…Prominent among these sets of genes are those traditionally associated with inflammation or, in the case of brain diseases, ''neuroinflammation'' (4,5). On histologic postmortem investigation, neurodegenerative disorders reveal pronounced changes in the functional state of glial cells with activation of both microglial cells and astrocytes (6)(7)(8)(9). The microglial activation process is associated with an increase in the number of microglial cells and the expression of numerous proteins (3)(4)(5).…”