Miyata M, Biro S, Kaieda H, Tanaka H
First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Japan.
FEBS Lett. 1995 Dec 27;377(3):493-6. doi: 10.1016/0014-5793(95)01404-7.
We investigated the effect of lipoprotein(a) (Lp(a)) on proliferation of human arterial smooth muscle cells (SMCs) and its mechanisms of action. Low density lipoprotein (LDL), Lp(a) and apolipoprotein(a) (apo(a)) significantly stimulated the proliferation of SMCs. Lp(a) and apo(a) reduced the amount of active transforming growth factor-beta (TGF-beta) with the mink lung epithelial cell bioassay, however LDL had no effect. Lp(a), but not apo(a), significantly stimulated the proliferation of SMCs even in the presence of a neutralizing antibody for TGF-beta. Our results suggest that Lp(a) stimulates the proliferation of SMCs via apo(a)-induced inhibition of TGF-beta activation and stimulation of SMCs by the LDL-particle of Lp(a).
我们研究了脂蛋白(a) [Lp(a)] 对人动脉平滑肌细胞 (SMC) 增殖的影响及其作用机制。低密度脂蛋白 (LDL)、Lp(a) 和载脂蛋白(a) [apo(a)] 显著刺激了 SMC 的增殖。采用貂肺上皮细胞生物测定法,Lp(a) 和 apo(a) 可减少活性转化生长因子-β (TGF-β) 的量,而 LDL 则无此作用。即使存在 TGF-β 中和抗体,Lp(a) 而非 apo(a) 仍能显著刺激 SMC 的增殖。我们的结果表明,Lp(a) 通过 apo(a) 诱导的 TGF-β 激活抑制以及 Lp(a) 的 LDL 颗粒对 SMC 的刺激来促进 SMC 的增殖。