PRODUCTION OF PLATELET-DERIVED GROWTH FACTOR-LIKE MOLECULES BY CULTURED ARTERIAL SMOOTH-MUSCLE CELLS ACCOMPANIES PROLIFERATION AFTER ARTERIAL INJURY

PRODUCTION OF PLATELET-DERIVED GROWTH FACTOR-LIKE MOLECULES BY CULTURED ARTERIAL SMOOTH-MUSCLE CELLS ACCOMPANIES PROLIFERATION AFTER ARTERIAL INJURY
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DOI:
10.1073/pnas.83.19.7311
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发表时间:
1986-10-01
影响因子:
11.1
通讯作者:
REIDY, MA
REIDY, MA
中科院分区:
综合性期刊1区
文献类型:
--
作者:
WALKER, LN;BOWENPOPE, DF;REIDY, MA

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机械损伤后动脉内膜内平滑肌细胞(SMC)的迁移和增殖被认为是由血管壁损伤和生长因子(特别是血小板衍生生长因子(PDGF))的释放引发的。然而,血小板与血管壁的相互作用停止后SMC增殖的调节机制尚不清楚。在这里,我们表明,平滑肌细胞来源于损伤的大鼠动脉内膜(内膜平滑肌细胞)是表型不同于平滑肌细胞从未经处理的血管(媒体平滑肌细胞)。内膜平滑肌细胞分泌5倍以上的PDGF样活性进入培养条件培养基中,具有较少的125 I标记的PDGF受体,并且不受外源性纯化PDGF的促有丝分裂刺激。这项研究表明,两种SMC表型可以在成年大鼠动脉中发展,并表明SMC在体内的增殖可能受到控制,在一定程度上,由SMC产生PDGF样分子。
The migration and proliferation of smooth muscle cells (SMCs) within the intima of arteries following mechanical injury is thought to be initiated by vessel wall injury and release of growth factors, in particular the platelet-derived growth factor (PDGF). However, the mechanism by which SMC proliferation is regulated after platelet interaction with the vessel wall has ceased is unknown. Here we show that SMCs derived from the intima of injured rat arteries (intimal SMCs) are phenotypically distinct from SMCs from unmanipulated vessels (media SMCs). Intimal SMCs secrete 5-fold greater amounts of PDGF-like activity into conditioned medium in culture, have fewer receptors for 125I-labeled PDGF, and are not mitogenically stimulated by exogenous purified PDGF. This study demonstrates that two SMC phenotypes can develop in the adult rat artery and suggests that SMC proliferation in vivo may be controlled, in part, by SMCs that produce PDGF-like molecules.