期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 279, 期 5, 页码 H2529-H2539出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2000.279.5.H2529
关键词
kinase activation; cell cycle; cell proliferation; arginine vasopressin
资金
- NCI NIH HHS [P30 CA-43703] Funding Source: Medline
- NHLBI NIH HHS [R01 HL-39757, P01 HL-41618] Funding Source: Medline
Arginine vasopressin (AVP) activation of V-1 vascular receptors (V(1)Rs) stimulates cell growth and proliferation in different tissues via cellular signaling pathways that remain to be identified. To explore the intracellular mediators of the mitogenic action of V1R, Chinese hamster ovary (CHO) cells were stably transfected with the human V1R cDNA clone we isolated previously. We assessed AVP effects on kinase activation (immunoblotting with phosphospecific antibodies), DNA synthesis (tritiated thymidine uptake), cell cycle progression (flow cytometry analysis after nuclear labeling with propidium iodide), and cell proliferation (conversion of the colorimetric reagent MTS) in the presence or absence of various pathway inhibitors. AVP stimulation of V(1)Rs leads to the phosphorylation of several kinases, an increase in DNA synthesis, a progression through the S and G(2)-M phases of the cell cycle, and an increase in cell proliferation. The mediators of the mitogenic action of V1R activation included calcium mobilization, coupling to a G(q) protein, and the simultaneous and parallel activation of several kinases, mainly calcium/calmodulin-dependent kinase II, phosphatidylinositol 3 kinase, protein kinase C, and p42/p44 mitogen-activated protein kinase.
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