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

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Abstract
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 Alexander9s disease, Alzheimer9s 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 α B-crystallin (αBC), both of which are members of sHSPs, in reactive astrocytes. In contrast, in vitrochemical ischemic stress induced both HSP27 and αBC in cultured glial cells to the same extent. Dibutyryl cAMP (dBcAMP) and isoproterenol, a β-adrenergic receptor (βAR) agonist, enhanced HSP27 expression but suppressed αBC, and changed the shape of the cells to a stellate form. dBcAMP and isoproterenol inhibited cell proliferation under normal conditions. An increase in βAR-like immunoreactivity was also observed in reactive astrocytes in vivo. These results, together with recent findings that βAR plays an important role in glial scar formation in vivo, raise the possibility that βAR activation modulates sHSP expression after focal ischemia and is involved in the transformation of astrocytes to their reactive form.