Yutaka Koyama1, Yuji Kimura1, Yasuhiro Yoshioka1,
Daisuke Wakamatsu1, Ryo-hei Kozaki1,
Hitoshi Hashimoto1, Toshio Matsuda2 and Akemichi Baba1,*
1Laboratory╩of Molecular Neuropharmacology and 2Laboratory of Medicinal Pharmacology,
Graduate School of Pharmaceutical Sciences, Osaka University, Yamada-Oka 1-6, Suita 565-0871, Japan
*╩To whom correspondence should be addressed.
Abstract: Expression of Bcl-2 related proteins in rat microglial primary culture was examined. At relative low cell densities, serum deprivation caused cell death and nuclei condensation of cultured microglia. Expression of a pro-apoptotic protein, Bax, but not Bcl-2, was increased by the serum deprivation. SB203580, a specific inhibitor of p38MAPK, prevented both the serum deprivation-induced Bax expression and microglial death. Immunochemical staining showed that microglia expressing a high level of Bax were subjected to apoptosis-like cell death. These observations suggest that Bax expression underlies the apoptosis of cultured microglia after serum deprivation.
Keywords: Microglia, Bax, Apoptosis
Copyrightę The Japanese Pharmacological Society 2000
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