Platelet-derived growth factor: its potential roles in wound healing, atherosclerosis, neoplasia, and growth and development.
Platelet-derived growth factor: its potential roles in wound healing, atherosclerosis, neoplasia, and growth and development.
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DOI：
10.1002/9780470720974.ch7
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
R. Ross;D. Bowen-Pope;E. Raines
中科院分区：
文献类型：
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作者：
R. Ross;D. Bowen-Pope;E. Raines
血小板衍生生长因子（PDGF）不仅来源于被诱导释放其内含物的血小板，而且来源于许多转化细胞（包括由DNA和RNA病毒转化的细胞、自发转化和来自各种人肿瘤的细胞），来自活化的巨噬细胞，来自胚胎大鼠主动脉平滑肌细胞，和来自实验诱导的内膜增生损伤的大鼠主动脉平滑肌细胞。所讨论的研究证明了血小板和巨噬细胞在动脉粥样硬化和伤口修复中的潜在作用，并表明抗PDGF IgG在体外抑制增殖反应的能力。由于证明了来源于猿肉瘤病毒的癌基因的转化蛋白与PDGF高度同源，因此有可能表明许多转化细胞分泌PDGF并显示出显著降低的PDGF结合。胚胎大鼠主动脉平滑肌细胞和大鼠颈动脉中实验诱导的增殖性病变细胞也是如此。所有这些发现都指出了PDGF在这些病变形成中的作用，并且可以与上述细胞以及受损的内皮细胞分泌PDGF或PDGF样分子的能力相关。这些观察结果的生物学意义进行了讨论，并提出了动脉粥样硬化模型。
Platelet-derived growth factor (PDGF) has been found to be derived not only from platelets that have been induced to release their contents, but also from a number of transformed cells (including cells transformed by both DNA and RNA viruses, spontaneous transformation, and cells from various human tumours), from activated macrophages, from embryonic rat aortic smooth muscle cells, and from rat aortic smooth muscle cells derived from experimentally induced intimal proliferative lesions. The studies discussed demonstrate the potential role of platelets and macrophages in atherosclerosis and in wound repair, and indicate the ability of anti-PDGF IgG to inhibit proliferative responses in vitro. With the demonstration that the transforming protein derived from the oncogene from the simian sarcoma virus is highly homologous with PDGF, it was possible to show that a number of transformed cells secrete PDGF and show markedly decreased binding of PDGF. The same is true for embryonic rat aortic smooth muscle cells and for cells from experimentally induced proliferative lesions in the rat carotid artery. All these findings point to the role of PDGF in the formation of these lesions and can be correlated with the capacity of the cells noted above, as well as injured endothelial cells, to secrete PDGF or PDGF-like molecules. The biological significance of these observations is discussed and a model for atherogenesis is proposed.