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Induction of heat shock proteins by hyperglycemic cerebral ischemia

Marianna Muranyi1, Qing Ping He, Keith S K Fong

  • 1Cardiovascular Research Center, John A. Burns School of Medicine, University of Hawaii, 1960 East West Road, Biomedical Tower 514, Honolulu, HI 96822, USA.

Brain Research. Molecular Brain Research
|June 18, 2005
PubMed

Insights

Hyperglycemia does not worsen ischemic brain damage by suppressing heat shock proteins (HSPs). Instead, hyperglycemic ischemia increased HSP70 and HSP60 levels, indicating a strong cellular stress response.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Molecular Biology

Background:

  • Diabetic hyperglycemia is known to worsen neuronal death following cerebral ischemia.
  • Previous research indicated that hyperglycemia suppressed heat shock protein 70 (HSP70) expression in the liver.

Purpose of the Study:

  • To investigate if hyperglycemia exacerbates ischemic brain damage by suppressing heat shock protein (HSP) expression in the brain.
  • To determine the role of HSPs in the context of hyperglycemic ischemia.

Main Methods:

  • Utilized a rat model of transient global cerebral ischemia under both normoglycemic and hyperglycemic conditions.
  • Analyzed the expression of stress-related genes using DNA microarray.
  • Quantified HSP protein levels via immunocytochemistry and Western blot analyses.

Main Results:

  • Hyperglycemic ischemia led to an upregulation of various heat shock protein genes, including hsp70, hsp90A, hsp90B, heat shock cognate 71 kD protein (hsc70), and mitochondrial hsp70 (mthsp70).
  • Protein levels of HSP70 and HSP60 were significantly enhanced in hyperglycemic rats compared to normoglycemic controls.
  • The study found no evidence that suppressed HSP expression mediates hyperglycemia-induced exacerbation of ischemic brain damage.

Conclusions:

  • Hyperglycemia-exacerbated ischemic brain damage is not caused by a suppression of heat shock proteins in the brain.
  • Elevated levels of HSPs and mthsp70 suggest a robust cellular and mitochondrial stress response to hyperglycemic ischemia.

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