Heparin inhibits proliferation of fetal vascular smooth muscle cells in the absence of platelet-derived growth factor.

Heparin inhibits proliferation of fetal vascular smooth muscle cells in the absence of platelet-derived growth factor.
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在缺乏血小板衍生生长因子的情况下,肝素可抑制胎儿血管平滑肌细胞的增殖。

DOI:
10.1002/jcp.1041270102
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发表时间:
1986
影响因子:
5.6
通讯作者:
Bernfield,M
Bernfield,M
中科院分区:
生物学2区
文献类型:
--
作者:
Benitz,WE;Lessler,DS;Coulson,JD;Bernfield,M

文献摘要

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肝素对胎犊肺动脉和主动脉平滑肌细胞增殖的抑制作用。这种效应是可逆的,并且是剂量依赖性的。与其他多糖作用的比较表明,只有广泛硫酸酸化的多糖才能抑制平滑肌细胞的增殖,但肝素的特定结构特征需要达到最大的效果。含有胎牛血清的培养基的肝素- Sepharose色谱降低了该培养基促进胎儿肺动脉平滑肌细胞生长的能力,表明肝素可能去除血清中的可溶性生长因子。然而,肝素对胎儿肺动脉平滑肌细胞增殖的抑制作用在两种培养基中是相同的,一种培养基中添加了从胎牛血浆制备的血清,其中未检测到血小板衍生生长因子(PDGF),另一种培养基中添加了含有相对丰富的PDGF (114 pg/ml)的胎牛血清。因此,肝素对胎儿肺动脉平滑肌细胞增殖的抑制并不仅仅是通过降低外源性PDGF的可用性或活性来介导的。这些研究表明,肺动脉平滑肌投资的形态发生可以通过局部产生平滑肌细胞生长的肝素样抑制剂来调节。
Proliferation of smooth muscle cells from the pulmonary arteries and aortas of fetal calves is inhibited by heparin in vitro. This effect is reversible and dose dependent. Comparisons with effects of other polysaccharides indicate that only extensively sulfated polysaccharides inhibit proliferation of smooth muscle cells but that specific structural features of heparin are required to achieve maximum effect. Heparin‐Sepharose chromatography of medium containing fetal calf serum reduces the ability of that medium to promote growth of smooth muscle cells from fetal pulmonary arteries, suggesting that heparin may remove soluble growth factors in serum. However, inhibition of fetal pulmonary artery smooth muscle cell proliferation by heparin is identical in media supplemented either with serum prepared from fetal calf plasma, in which platelet‐derived growth factor (PDGF) is not detectable, or with fetal calf serum, which contains relatively abundant PDGF (114 pg/ml). Thus, inhibition of fetal pulmonary artery smooth muscle cell proliferation by heparin is not mediated solely by decreased availability or activity of exogenous PDGF. These studies suggest that morphogenesis of the smooth muscle investment of the pulmonary arteries could be regulated by local production of heparinlike inhibitors of smooth muscle cell growth.