Järveläinen H, Halme T, Lehtonen A, Rönnemaa T
Atherosclerosis. 1985 Aug;56(2):199-211. doi: 10.1016/0021-9150(85)90019-x.
The effect of serum from type IIA hyperlipoproteinemic patients on the proliferation and synthesis of collagen and other proteins of human fetal aortic smooth muscle cells (SMC) was studied. The activity of lysyl oxidase secreted into the culture medium was also measured. Type IIA hyperlipoproteinemic sera did not affect the proliferation of human aortic SMC as compared to normolipidemic sera, regardless of incubation time. The findings were similar for 3 different human fetal aortic SMC lines and one fibroblast line from adult human skin. The synthesis of collagen and other proteins was inhibited rather than stimulated in the presence of type IIA hyperlipoproteinemic sera. The activity of lysyl oxidase was not affected by type IIA hyperlipoproteinemic sera. The atherogenicity of hypercholesterolemia cannot be explained either by its direct effect on the proliferation of arterial SMC, as has been suggested by animal cell studies, or by its direct effect on the fibrogenicity of these cells.
研究了IIA型高脂蛋白血症患者血清对人胎儿主动脉平滑肌细胞（SMC）增殖以及胶原蛋白和其他蛋白质合成的影响。还测定了分泌到培养基中的赖氨酰氧化酶的活性。与正常血脂血清相比，无论孵育时间长短，IIA型高脂蛋白血症血清均不影响人主动脉SMC的增殖。3种不同的人胎儿主动脉SMC系和1种成人皮肤成纤维细胞系的研究结果相似。在IIA型高脂蛋白血症血清存在的情况下，胶原蛋白和其他蛋白质的合成受到抑制而非刺激。IIA型高脂蛋白血症血清不影响赖氨酰氧化酶的活性。高胆固醇血症的致动脉粥样硬化性既不能像动物细胞研究所表明的那样，通过其对动脉SMC增殖的直接作用来解释，也不能通过其对这些细胞纤维化形成的直接作用来解释。
