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首页> 外文期刊>Journal of vascular research >Low- and high-density lipoproteins as mitogenic factors for vascular smooth muscle cells: individual, additive and synergistic effects.
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Low- and high-density lipoproteins as mitogenic factors for vascular smooth muscle cells: individual, additive and synergistic effects.

机译：低密度脂蛋白和高密度脂蛋白是血管平滑肌细胞的促有丝分裂因子：个体，累加和协同作用。

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摘要

The mitogenic activities of low (LDL)- and high (HDL)-density lipoproteins have been examined in cultures of human vascular smooth muscle cells (VSMC). LDL and HDL3 dose-dependently (EC50 values approximately 50 micrograms/ml) stimulated DNA and protein synthesis ([3H]-thymidine and [3H]-leucine incorporation, respectively) in the absence of exogenously added mitogens. The synthetic responses of VSMC to combinations of LDL and HDL3 were additive, indicating that each lipoprotein mediates discrete effects. LDL or HDL3 promoted VSMC proliferation under strict mitogen-free conditions, but this growth response was not sustained. VSMC exposed to combinations of lipoproteins (either LDL or HDL3) and growth factors (either PDGF-BB, EGF, bFGF or IGF) exhibited synergistic DNA synthesis responses. In the combined presence of PDGF-BB and either LDL or HDL3, VSMC proliferation was sustained. Anionized lipoprotein preparations (oxidized, acetylated, carbamylated or malonimylated) also stimulated DNA and protein synthesis. Since the antioxidant beta-hydroxylated toluene did not block the effect of native LDL on DNA synthesis, and fucoidin, a specific competitor for the 'scavenger' receptor, did not inhibit oxidized LDL-induced DNA synthesis, activation of mitogenic signals by lipoproteins does not depend on lipid peroxidation. Rather, the apparent intrinsic mitogenic potential of lipoproteins may depend upon their direct activation of replication-coupled signal transduction systems.
机译：低密度脂蛋白和高密度脂蛋白的促有丝分裂活性已在人血管平滑肌细胞（VSMC）的培养物中进行了检查。 LDL和HDL3剂量依赖性地（EC50值约为50微克/毫升）刺激了DNA和蛋白质的合成（分别[3H]-胸苷和[3H]-亮氨酸掺入），而没有外源添加的促细胞分裂剂。 VSMC对LDL和HDL3组合的合成反应是累加的，表明每种脂蛋白介导离散作用。 LDL或HDL3在严格的无促分裂原条件下促进VSMC增殖，但这种增长反应并未持续。暴露于脂蛋白（LDL或HDL3）和生长因子（PDGF-BB，EGF，bFGF或IGF）组合的VSMC表现出协同的DNA合成反应。在PDGF-BB和LDL或HDL3的共同存在下，VSMC的增殖得以持续。阴离子化脂蛋白制剂（氧化，乙酰化，氨基甲酰化或丙二酸化）也刺激了DNA和蛋白质的合成。由于抗氧化剂β-羟基化的甲苯不会阻止天然LDL对DNA合成的影响，而岩藻依糖苷（“清道夫”受体的特定竞争者）不会抑制氧化的LDL诱导的DNA合成，因此脂蛋白不会激活有丝分裂信号取决于脂质过氧化。而是，脂蛋白的表观固有有丝分裂潜力可能取决于它们对复制偶联信号转导系统的直接激活。

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