Bradykinin stimulates the tyrosine phosphorylation and bradykinin B2 receptor association of phospholipase C gamma 1 in vascular endothelial cells.
Bradykinin stimulates the tyrosine phosphorylation and bradykinin B2 receptor association of phospholipase C gamma 1 in vascular endothelial cells.
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缓激肽刺激血管内皮细胞中磷脂酶 C gamma 1 的酪氨酸磷酸化和缓激肽 B2 受体关联。
DOI：
10.1006/bbrc.1998.8574
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Venema,RC
中科院分区：
文献类型：
--
作者：
Venema,VJ;Ju,H;Sun,J;Eaton,DC;Marrero,MB;Venema,RC
缓激肽（BK）B2受体信号传导涉及磷脂酶C（PLC）的活化。其他受体对PLC的激活包括G蛋白对PLCβ亚型的变构激活或PLCγ亚型的酪氨酸磷酸化。由于B2受体是一种G蛋白偶联受体，因此假设该受体通过PLCβ发出信号。然而，在本研究中，我们发现BK刺激内皮细胞产生IP 3和Ca 2+信号依赖于酪氨酸磷酸化。此外，这些细胞中B2受体的刺激伴随着PLCγ1的瞬时酪氨酸磷酸化。磷酸化与增加的IP 3产生和PLCγ1与B2受体的C-末端胞内结构域的缔合相关。因此，B2受体可以与G蛋白以外的细胞内蛋白质物理结合。因此，PLCγ亚型的激活，而不是PLCβ亚型的激活，可能是BK刺激内皮细胞产生IP 3的主要原因。
Bradykinin (BK) B2 receptor signaling involves activation of phospholipase C (PLC). PLC activation by other receptors consists of either allosteric activation of PLCβ isoforms by G-proteins or tyrosine phosphorylation of PLCγ isoforms. Because the B2 receptor is a G-protein-coupled receptor, it has been assumed that the receptor signals through PLCβ. In the present study, however, we have found that BK stimulation of IP3production and the Ca2+signal in endothelial cells is dependent on tyrosine phosphorylation. Furthermore, stimulation of B2 receptors in these cells is accompanied by a transient tyrosine phosphorylation of PLCγ1. Phosphorylation is correlated with increased IP3production and association of PLCγ1 with the C-terminal intracellular domain of the B2 receptor. The B2 receptor can thus physically associate with intracellular proteins other than G-proteins. Activation of PLCγ isoforms, rather than PLCβ isoforms, may, therefore, be primarily responsible for BK-stimulated IP3generation in endothelial cells.