Yamamoto H, Crow M, Cheng L, Lakatta E, Kinsella J
Laboratory of Cardiovascular Sciences, National Institute on Aging, National Institute of Health, Baltimore, Maryland 21224, USA.
Exp Cell Res. 1996 Jan 10;222(1):125-30. doi: 10.1006/excr.1996.0016.
Vascular smooth muscle cells (VSMC) are the predominant cell type in the media of a normal artery. Injury to the vessel wall leads to platelet deposition and the release of numerous factors, including PDGF, which exerts its biological effects by binding to specific surface receptors on the smooth muscle cell membrane. We demonstrate that PDGF-stimulated smooth muscle cells activate the STAT (signal transducers and activators of transcription) family of proteins in addition to other signaling pathways (e.g., RAS-RAF-MAP Kinase). We show that the transcription factor p91 (STAT1 alpha) is rapidly activated by PDGF in VSMC and specifically binds to the regulatory elements SIE or GAS. We hypothesize that signal transduction by p91 plays an important role in VSMC, especially after injury with the release of growth factors such as PDGF.
血管平滑肌细胞(VSMC)是正常动脉中层的主要细胞类型。血管壁损伤会导致血小板沉积并释放多种因子,包括血小板衍生生长因子(PDGF),它通过与平滑肌细胞膜上的特定表面受体结合来发挥其生物学效应。我们证明,血小板衍生生长因子刺激的平滑肌细胞除了激活其他信号通路(如RAS-RAF-丝裂原活化蛋白激酶)外,还会激活信号转导及转录激活蛋白(STAT)家族蛋白。我们发现,转录因子p91(STAT1α)在血管平滑肌细胞中被血小板衍生生长因子快速激活,并特异性结合到调控元件SIE或GAS上。我们推测,p91介导的信号转导在血管平滑肌细胞中起重要作用,尤其是在损伤后生长因子如血小板衍生生长因子释放时。