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首页> 外文期刊>Life sciences >Homocysteine potentiates calcification of cultured rat aortic smooth muscle cells.
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Homocysteine potentiates calcification of cultured rat aortic smooth muscle cells.

机译：同型半胱氨酸增强培养的大鼠主动脉平滑肌细胞的钙化。

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Aortic calcification was demonstrated in experimental animal models of hyperhomocysteinemia. Mild hyperhomocysteinemia was associated with aortic calcification, suggesting a relationship between homocysteine (HCY) and the pathogenesis of aortic calcification. In the present study, the effect of HCY on vascular calcification was examined in calcifying and non-calcifying vascular smooth muscle cells (VSMCs). Cell calcification was induced by incubation of VSMCs with beta-glycerophosphate. Proliferation of VSMCs was studied by cell counting, 3H-thymidine (3H-TdR) and 3H-leucine (3H-Leu) incorporation. 45Ca accumulation, cell calcium content, and alkaline phosphatase (ALP) activity were measured as indices of calcification. The results showed that the proliferation of calcifying VSMCs, which was indicated by cell counting, 3H-TdR and 3H-Leu incorporation in calcifying VSMCs, was enhanced as compared with that of non-calcifying VSMCs. HCY promoted increases in cell number, 3H-TdR and 3H-Leu incorporation inboth calcifying and non-calcifying VSMCs, but with more prominent effect in calcifying VSMCs. The stimulating effects of HCY on the three parameters in calcifying VSMCs were antagonized by PD98059, a specific inhibitor of mitogen activated protein kinase kinase (MAPKK). The ALP activity, 45Ca uptake, and calcium deposition in the calcifying VSMCs were greater than those in non-calcifying VSMCs. PD98059 had no effect on ALP activity, 45Ca uptake, and calcium deposition in calcifying VSMCs. HCY caused marked increases in 45Ca uptake and calcium deposition both in calcifying and non-calcifying VSMCs. HCY, however, enhanced ALP activity in the calcified VSMCs but not in the non-calcifying VSMCs. The non-calcifying VSMCs treated with HCY showed the same low ALP activity, as did the control VSMCs. In calcifying VSMCs, the HCY-induced increases in 45Ca uptake, calcium deposition, and ALP activity were also attenuated by PD98059. The results demonstrated that HCY potentiated VSMC calcification probably through the mechanisms by which HCY promotes atherosclerosis.
机译：在高同型半胱氨酸血症的实验动物模型中证明了主动脉钙化。轻度高同型半胱氨酸血症与主动脉钙化有关，提示同型半胱氨酸（HCY）与主动脉钙化的发病机理之间存在关联。在本研究中，在钙化和非钙化血管平滑肌细胞（VSMC）中检查了HCY对血管钙化的影响。通过将VSMC与β-甘油磷酸一起孵育来诱导细胞钙化。通过细胞计数，3H-胸苷（3H-TdR）和3H-亮氨酸（3H-Leu）掺入研究了VSMC的增殖。测量45Ca积累，细胞钙含量和碱性磷酸酶（ALP）活性作为钙化的指标。结果表明，与非钙化VSMC相比，通过细胞计数，3H-TdR和3H-Leu掺入钙化VSMC表明钙化VSMC的增殖得到增强。 HCY促进钙化和非钙化VSMC中细胞数量，3H-TdR和3H-Leu掺入的增加，但在钙化VSMC中具有更显着的作用。 H980对钙化VSMC的三个参数的刺激作用被有丝分裂原激活的蛋白激酶激酶（MAPKK）的特异性抑制剂PD98059拮抗。钙化型VSMC中的ALP活性，45Ca摄取和钙沉积均大于非钙化型VSMC。 PD98059对钙化VSMC中的ALP活性，45Ca摄取和钙沉积没有影响。在钙化和非钙化的VSMC中，HCY引起45Ca吸收和钙沉积的显着增加。但是，HCY在钙化的VSMC中增强了ALP活性，但在非钙化的VSMC中却没有增强。用HCY处理的非钙化VSMC与对照VSMC表现出相同的低ALP活性。在钙化VSMC中，PD98059还减弱了HCY诱导的45Ca吸收，钙沉积和ALP活性的增加。结果表明，HCY可能通过HCY促进动脉粥样硬化的机制增强了VSMC钙化。

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