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Angiogenin depresses aortic smooth muscle cell cAMP by a pertussis toxin sensitive mechanism.

作者信息

Xiao Y, Bicknell R, Vallee B L

机构信息

Center for Biochemical and Biophysical Sciences and Medicine, Harvard Medical School, Boston, MA 02115.

出版信息

Biochem Biophys Res Commun. 1989 Sep 15;163(2):902-7. doi: 10.1016/0006-291x(89)92307-3.

Abstract

Angiogenin transiently depresses the cAMP level of rat aortic smooth muscle cells. The dose response is similar to angiogenin activation of the inositol-specific phospholipase C in this cell line [Moore, F. & Riordan, J.F. (1989) Biochemistry. Submitted]. The time course showed a maximal depression (28%) in cAMP at 2 min, followed by a return to that of unstimulated cells by 3.5 min. Angiogenin also inhibited isoproterenol stimulated cAMP formation, but the percentage depression in cAMP (9%) was less than that in cells treated with angiogenin alone (28%). In contrast angiogenin enhanced forskolin stimulation of adenylate cyclase, an effect previously linked with agonist activation of protein kinase C. The effect of angiogenin on cellular cAMP was abolished by pre-incubation with pertussis toxin. Angiogenin had no effect on cellular cGMP. These results are consistent with activation of adenylate cyclase Gi following exposure of the cells to angiogenin and provide further evidence for interaction between cellular signalling pathways.

摘要

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