Saitoh O, Saitoh Y, Nakata H
Department of Molecular and Cellular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Japan.
Neuroreport. 1994 Jun 27;5(11):1317-20.
Modulation of A2a adenosine receptor (A2aAR) expression by adenosine agonists was studied in cultured PC12 cell lines. Exposure of A2aAR agonists such as 5'-N-ethylcarboxamidoadenosine (NECA) or CGS-21680 caused a transient increase followed by a decrease of A2aAR mRNA in PC12 cells in 10 h. This was followed by a gradual recovery to control levels by approximately 24 h. These changes were blocked by an adenosine receptor antagonist, xanthine amine congener. Forskolin also induced similar changes in the level of A2aAR mRNA. In addition, A2aAR numbers of PC12 cell membranes were significantly decreased during the NECA-exposure. These results suggest that A2aAR gene expression in PC12 cells is regulated by activation of A2aAR via a mechanism involving the second messenger, cAMP.
在培养的PC12细胞系中研究了腺苷激动剂对A2a腺苷受体（A2aAR）表达的调节作用。用5'-N-乙基羧基酰胺腺苷（NECA）或CGS-21680等A2aAR激动剂处理PC12细胞10小时后，A2aAR mRNA先出现短暂增加，随后减少。到约24小时时逐渐恢复到对照水平。腺苷受体拮抗剂黄嘌呤胺同类物可阻断这些变化。福斯高林也诱导A2aAR mRNA水平发生类似变化。此外，在NECA处理期间，PC12细胞膜上的A2aAR数量显著减少。这些结果表明，PC12细胞中A2aAR基因表达是通过涉及第二信使cAMP的机制，由A2aAR的激活来调节的。
