BioGPS
  • Home
  • Help
  • Plugins
  • Datasets
  • Sign Up
  • Login
Examples: Gene Symbol(s), Gene Ontology, Splicing plugins, Melanoma datasets
advanced
Home › Dataset Library › Effects of Hsp72 on astrocyte activation following stroke in the mouse

Dataset: Effects of Hsp72 on astrocyte activation following stroke in the mouse

Astrogliosis is a hallmark of the response to brain ischemia, comprised of changes in gene expression and morphology. Hsp72 protects from...

Registered by ArrayExpress Uploader
View Dataset

Astrogliosis is a hallmark of the response to brain ischemia, comprised of changes in gene expression and morphology. Hsp72 protects from cerebral ischemia, and although several mechanisms of protection have been investigated, effects on astrocyte activation are unknown. To identify potential mechanisms of protection, gene expression was assessed in mice subjected to middle cerebral artery (MCAO) or sham surgery, of either wildtype (WT) or Hsp72-overexpressing (Hsp72Tg) mice. After stroke, both genotypes exhibited genes related to cell death, stress response, and immune response. Furthermore, genes indicative of astrocyte activation, including cytoskeletal proteins and cytokines, were upregulated. To measure astrocyte activation after stroke, detailed histological and morphological analyses were performed in the cortical penumbra after stroke using unbiased stereology. Consistent with other reports, we observed a marked and persistent increase in glial fibrillary acidic protein (GFAP ) as soon as 3 hours after MCAO. In contrast, vimentin immunoreactivity appeared 12-24 hours after stroke, peaked at 72 hours, and returned to baseline after 30 days. Surprisingly, no change in overall astrocyte number was observed based on glutamine synthetase (GS) immunoreactivity. To determine if Hsp72Tg mice exhibited altered astrocyte activation compared to WT controls, morphological evaluation by fractal analysis was used. Overexpression of Hsp72 reduced astrocyte cell area, arbor area, and to a lesser extent fractal dimension, 72 hours following stroke. In conclusion, in vivo overexpression of Hsp72 alters gene expression following stroke, including genes involved in astrocyte activation, and decreases astrocyte activation acutely following MCAO. Thus, modulation of astrogliosis may be a neuroprotective mechanism exerted by Hsp72 after ischemia. A total of 10 samples were analyzed, with 5 of each genotype, wildtype (WT) and Hsp72-overexpressing (Hsp72Tg) mice. Of the 5 in each group, 3 received middle cerebral artery occlusion (MCAO) and 2 received a sham surgery. The sham samples serve as the controls for the MCAO samples in each genotype. All samples were taken from the ischemic or control hemisphere 24 hours after surgery.

Species:
mouse

Samples:
10

Source:
E-GEOD-28731

PubMed:
22940431

Updated:
Dec.12, 2014

Registered:
Nov.11, 2014


Factors: (via ArrayExpress)
Sample HEMISPHERE GENOTYPE TREATMENT
GSM711828 control WT sham
GSM711828 control WT sham
GSM711830 control Hsp72Tg sham
GSM711830 control Hsp72Tg sham
GSM711832 Ischemic WT MCAO
GSM711832 Ischemic WT MCAO
GSM711832 Ischemic WT MCAO
GSM711835 Ischemic Hsp72Tg MCAO
GSM711835 Ischemic Hsp72Tg MCAO
GSM711835 Ischemic Hsp72Tg MCAO

Tags

  • artery
  • astrocyte
  • brain
  • brain ischemia
  • cell
  • cerebral artery occlusion
  • glutamine
  • ischemia
  • middle
  • middle cerebral artery
  • protein
  • stroke
  • vimentin

Other Formats

JSON    XML
  • About
  • Blog
  • Help
  • FAQ
  • Downloads
  • API
  • iPhone App
  • Email updates
© 2025 The Scripps Research Institute. All rights reserved. (ver 94eefe6 )
  • Terms of Use