Di Salvo J, Raatz Nelson S
Department of Physiology, University of Minnesota, Minneapolis 55455, USA.
FEBS Lett. 1998 Jan 23;422(1):85-8. doi: 10.1016/s0014-5793(97)01606-2.
It is often believed that increases in intracellular Ca2+ ([Ca2+]i) resulting from stimulation of G-protein coupled receptors in vascular smooth muscle cells (VSMC) require activation of the beta1 isoform of phospholipase C (PLC). However, recent studies showed that rat aortic VSMC do not express PLC beta-1 and that stimulation with angiotensin-II induces tyrosine kinase dependent increases in [Ca2+]i and tyrosine phosphorylation of PLC gamma-1. Whether this pathway is activated by other vasoactive agents that stimulate G-protein coupled receptors is unknown. Here, we show that A10 VSMC express PLC beta-2, PLC beta-3, PLC delta-1, and PLC gamma-1. The cells also expressed Galpha(q/11). However, neither PLC beta-1 nor PLC beta-4 was detected. Stimulation with angiotensin-II, vasopressin, serotonin, or endothelin induced tyrosine kinase dependent increases in [Ca2+]i. However, tyrosine phosphorylation of PLC gamma-1 did not occur. In contrast, stimulation with platelet derived growth factor increased [Ca2+]i and tyrosine phosphorylation of PLC gamma-1. The results show that tyrosine phosphorylation of PLC gamma-1 is not required for tyrosine kinase dependent increases in [Ca2+]i resulting from stimulation of diverse G-protein coupled receptors in VSMC.
人们通常认为，血管平滑肌细胞（VSMC）中因G蛋白偶联受体受刺激而导致的细胞内Ca2+（[Ca2+]i）增加需要磷脂酶C（PLC）的β1亚型激活。然而，最近的研究表明，大鼠主动脉VSMC不表达PLCβ - 1，并且血管紧张素 - II刺激会诱导酪氨酸激酶依赖性的[Ca2+]i增加以及PLCγ - 1的酪氨酸磷酸化。该途径是否被其他刺激G蛋白偶联受体的血管活性药物激活尚不清楚。在这里，我们表明A10 VSMC表达PLCβ - 2、PLCβ - 3、PLCδ - 1和PLCγ - 1。这些细胞也表达Gα(q/11)。然而，未检测到PLCβ - 1和PLCβ - 4。血管紧张素 - II、血管加压素、血清素或内皮素刺激会诱导酪氨酸激酶依赖性的[Ca2+]i增加。然而，PLCγ - 1的酪氨酸磷酸化并未发生。相反，血小板衍生生长因子刺激会增加[Ca2+]i和PLCγ - 1的酪氨酸磷酸化。结果表明，VSMC中因多种G蛋白偶联受体受刺激而导致的酪氨酸激酶依赖性[Ca2+]i增加并不需要PLCγ - 1的酪氨酸磷酸化。
