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首页> 外文期刊>EMBO Journal >Urokinase-induced signaling in human vascular smooth muscle cells is mediated by PDGFR-beta
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Urokinase-induced signaling in human vascular smooth muscle cells is mediated by PDGFR-beta

机译:在人类血管Urokinase-induced信号平滑肌细胞是由PDGFR-beta介导的

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摘要

Urokinase (uPA)-induced signaling in human vascular smooth muscle cells (VSMC) elicits important cellular functional responses, such as cell migration and proliferation. However, how intracellular signaling is linked to glycolipid-anchored uPA receptor (uPAR) is unknown. We provide evidence that uPAR activation by uPA induces its association with platelet-derived growth factor receptor (PDGFR)-beta. The interaction results in PDGF-independent PDGFR-beta activation by phosphorylation of cytoplasmic tyrosine kinase domains and receptor dimerization. Association of the receptors as well as the tyrosine kinase activity of PDGFR-beta are decisive in mediating uPA-induced downstream signaling that regulates VSMC migration and proliferation. These findings provide a molecular basis for mechanisms VSMC use to induce uPAR- and PDGFR-directed signaling. The processes may be relevant to VSMC function and vascular remodeling.
机译:全身的尿激酶(uPA)信号在人类血管平滑肌细胞(VSMC)引出重要的细胞功能反应,例如细胞的迁移和增殖能力。细胞内信号传导有关glycolipid-anchored uPA受体(uPAR)未知的。uPA诱发其协会血小板源生长因子受体(PDGFR)β。PDGF-independent PDGFR-beta激活的胞质酪氨酸激酶的磷酸化域和受体二聚作用。酪氨酸激酶受体以及活动PDGFR-beta果断在调停uPA-induced下游信号调节VSMC迁移和增殖。机制提供分子依据VSMC使用诱导uPAR PDGFR-directed信号。流程与VSMC的功能和相关的可能血管重建。

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