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血清脂蛋白组成、血小板因子与动脉平滑肌细胞。

Serum lipoprotein composition, platelet factor and arterial smooth muscle cells.

作者信息

Rönnemaa T

出版信息

Acta Med Scand Suppl. 1980;642:55-65. doi: 10.1111/j.0954-6820.1980.tb10936.x.

DOI:10.1111/j.0954-6820.1980.tb10936.x
PMID:7006328
Abstract

The incorporation of [3H] thymidine and the synthesis of glycosaminoglycans (GAG) by cultured human aortic smooth muscle cells were studied in the presence of human sera with high HDL cholesterol concentration, high LDL cholesterol concentration or with normal serum lipoprotein concentrations. The sera were prepared either conventionally (CPS, platelet factor present) or from platelet poor plasma by recalcification (PPPS). As compared to normolipidaemic sera, HDL-aemic CPS decreased the incorporation of thymidine but LDL-aemic sera had no effect. HDL-aemic sera decreased markedly the synthesis of sulphated GAG but had no effect on the synthesis of hyaluronic acid (HA). Therefore, the sulphated GAG/HA ratio was decreased. The decrease in sulphated GAG was observed only in the presence of CPS, not in the presence of PPPS. LDL-aemic sera decreased the synthesis of hyaluronic acid causing an increase in the sulphated GAG/HA ratio. This effect was observed in the presence of both CPS and PPPS. The results suggest that determination of the sulphated GAG/HA ratio in aortic smooth muscle cell cultures provides a useful method for estimating the atherogeneity of various sera. The anti-atherogenic effect of HDL-aemic sera seems to be dependent on the platelet factor while the atherogenic effect of LDL-aemic sera may be independent of the platelet factor.

摘要

在含有高HDL胆固醇浓度、高LDL胆固醇浓度或正常血清脂蛋白浓度的人血清存在的情况下,研究了培养的人主动脉平滑肌细胞中[3H]胸苷的掺入和糖胺聚糖(GAG)的合成。血清要么通过常规方法制备(CPS,存在血小板因子),要么通过再钙化从乏血小板血浆制备(PPPS)。与正常血脂血清相比,HDL血症CPS降低了胸苷的掺入,但LDL血症血清没有影响。HDL血症血清显著降低了硫酸化GAG的合成,但对透明质酸(HA)的合成没有影响。因此,硫酸化GAG/HA比值降低。仅在CPS存在时观察到硫酸化GAG的降低,而在PPPS存在时未观察到。LDL血症血清降低了透明质酸的合成,导致硫酸化GAG/HA比值增加。在CPS和PPPS存在时均观察到这种效应。结果表明,测定主动脉平滑肌细胞培养物中的硫酸化GAG/HA比值为评估各种血清的动脉粥样硬化性提供了一种有用的方法。HDL血症血清的抗动脉粥样硬化作用似乎依赖于血小板因子,而LDL血症血清的动脉粥样硬化作用可能与血小板因子无关。

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