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The Journal of Neuroscience, November 15, 1999, 19(22):9768-9779

Differential Expression of Small Heat Shock Proteins in Reactive Astrocytes after Focal Ischemia: Possible Role of -Adrenergic Receptor

Tetsuya Imura¹, Shun Shimohama¹, Masaaki Sato², Hiroyuki Nishikawa², Kenya Madono², Akinori Akaike², and Jun Kimura¹

¹ Department of Neurology, Graduate School of Medicine, and ² Department of Pharmacology, Graduate School of Pharmaceutical Science, Kyoto University, Kyoto 606-8507, Japan

Small heat shock proteins (sHSPs), a family of HSPs, are known to accumulate in the CNS, mainly in astrocytes, in several pathological conditions such as Alexander's disease, Alzheimer's disease, and Creutzfeldt-Jakob disease. sHSPs may act not only as molecular chaperones, protecting against various stress stimuli, but may also play a physiological role in regulating cell differentiation and proliferation. In the present study, we have demonstrated that transient focal ischemia in rats dramatically induced HSP27 but not  B-crystallin (BC), both of which are members of sHSPs, in reactive astrocytes. In contrast, in vitro chemical ischemic stress induced both HSP27 and BC in cultured glial cells to the same extent. Dibutyryl cAMP (dBcAMP) and isoproterenol, a -adrenergic receptor (AR) agonist, enhanced HSP27 expression but suppressed BC, and changed the shape of the cells to a stellate form. dBcAMP and isoproterenol inhibited cell proliferation under normal conditions. An increase in AR-like immunoreactivity was also observed in reactive astrocytes in vivo. These results, together with recent findings that AR plays an important role in glial scar formation in vivo, raise the possibility that AR activation modulates sHSP expression after focal ischemia and is involved in the transformation of astrocytes to their reactive form.

Key words: small heat shock proteins; ischemia; reactive astrocytes; -adrenergic receptor; glia; cell differentiation

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19229768-12$05.00/0

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