Oikawa S, Hori S, Sano R, Suzuki N, Fujii Y, Abe R, Goto Y
Atherosclerosis. 1987 Mar;64(1):7-12. doi: 10.1016/0021-9150(87)90048-7.
Increased concentration of plasma low-density lipoprotein (LDL) is one of the risk factors in atherosclerosis. We studied how DNA synthesis of human arterial smooth muscle cells (SMC) was influenced in the culture added with or without small dose (25 micrograms of protein/ml) of LDL. LDL were ultracentrifugally obtained from normal subjects and diabetics. DNA synthesis was investigated at 6-h intervals during 36 h in the culture with or without LDL using [methyl-3H]thymidine. We found that DNA synthesis reached a maximum value at 24 h after addition of LDL. On the other hand sequential changes were not detectable in the culture without LDL addition. This effect of diabetic LDL was significantly (P less than 0.001) greater than that of normal LDL. These results suggested that LDL induces synchronization of the cultured SMC to synthesize DNA and diabetic LDL may play an atherogenic role more strongly than normal LDL in the arterial wall even in the normal range of LDL concentration.
血浆低密度脂蛋白（LDL）浓度升高是动脉粥样硬化的危险因素之一。我们研究了在添加或不添加小剂量（25微克蛋白质/毫升）LDL的培养物中，人动脉平滑肌细胞（SMC）的DNA合成是如何受到影响的。LDL通过超速离心从正常受试者和糖尿病患者中获得。使用[甲基-3H]胸腺嘧啶核苷，在添加或不添加LDL的培养物中，每隔6小时研究36小时内的DNA合成情况。我们发现，添加LDL后24小时，DNA合成达到最大值。另一方面，在未添加LDL的培养物中未检测到连续变化。糖尿病患者的LDL的这种作用明显（P<0.001）大于正常LDL。这些结果表明，LDL诱导培养的SMC同步合成DNA，即使在LDL浓度正常范围内，糖尿病患者的LDL在动脉壁中可能比正常LDL更强烈地发挥致动脉粥样硬化作用。
