INDUCTION OF HEME OXYGENASE-1 AND MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS IN TRANSIENT FOREBRAIN ISCHEMIA

Recent studies strongly suggest that oxidative stresses participate in ischemia/reperfusion-induced neurodegeneration. In addition, heme oxy genase (HO) and major histocompatibility complex (MHC) antigens serve as functional molecules against oxidative stress and as self-recogniti on markers in the immune system, respectively. In this study, we exami ned the induction of HO and MHC antigens in the rat hippocampus after transient forebrain ischemia, The protein level of HO-1 was significan tly enhanced after an episode of ischemia. After ischemia, HO-1 expres sion was observed early but transiently in the CA1 pyramidal neurons a nd later but continuously in glial cells. Glial cells expressing HO-1 were predominantly ameboid microglia, but not astrocytes. Ameboid micr oglia expressing HO-1 were predominantly localized with MHC class II a ntigens. These results indicate that (1) HO-1 expression in CAI pyrami dal neurons may be harmful, and (2) ischemia induces HO-1 in ameboid m icroglia that express MHC class II antigens, indicating a very specifi c microglial stress protein response.