Taniguchi T, Nemoto Y, Ota K, Imai T, Tobari J
Medical Research Laboratory, Kochi Medical School, Japan.
Biochem Biophys Res Commun. 1993 Jun 30;193(3):886-9. doi: 10.1006/bbrc.1993.1708.
We previously demonstrated that the expression of a transfected poly(ADP-ribose) synthetase cDNA into macrophage tumor cells inhibited interferon-gamma-dependent induction of major histocompatibility complex(MHC) class II antigens. In the present study, we found that addition of norepinephrine to the cultured human astrocytoma STTG1 cells induced mRNA of poly(ADP-ribose) synthetase in 6-14h. Thus, we cultured the cells in the presence of norepinephrine for 24h, and then induced the MHC class II antigen by the addition of interferon-gamma. The expression of MHC class II antigen was inhibited, whereas it was not inhibited when norepinephrine and interferon-gamma were simultaneously added into the culture medium. These results suggest that an increase of poly(ADP-ribose) synthetase by norepinephrine cause the inhibition of interferon-gamma-mediated MHC class II antigen expression.
我们先前证明，将转染的聚（ADP - 核糖）合成酶cDNA导入巨噬细胞肿瘤细胞后，会抑制γ干扰素依赖的主要组织相容性复合体（MHC）II类抗原的诱导。在本研究中，我们发现向培养的人星形细胞瘤STTG1细胞中添加去甲肾上腺素会在6 - 14小时内诱导聚（ADP - 核糖）合成酶的mRNA。因此，我们在去甲肾上腺素存在的情况下培养细胞24小时，然后通过添加γ干扰素诱导MHC II类抗原。MHC II类抗原的表达受到抑制，而当将去甲肾上腺素和γ干扰素同时添加到培养基中时，其表达未受到抑制。这些结果表明，去甲肾上腺素导致的聚（ADP - 核糖）合成酶增加会抑制γ干扰素介导的MHC II类抗原表达。
