Promotion of Aortic Smooth Muscle Cell Proliferation by Hypercholesterolemic LDL and Its Suppression by Heparin or Sulfated Glycosaminoglycans
Promotion of Aortic Smooth Muscle Cell Proliferation by Hypercholesterolemic LDL and Its Suppression by Heparin or Sulfated Glycosaminoglycans
复制标题
高胆固醇血症 LDL 促进主动脉平滑肌细胞增殖及其肝素或硫酸化糖胺聚糖的抑制作用
DOI：
10.1159/000154709
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发表时间：
1994
影响因子：
--
通讯作者：
T. Tulenko
中科院分区：
文献类型：
--
作者：
H. Tasaki;Y. Nakashima;J. Segawa;R. Kouzuma;A. Kuroiwa;D. Sparks;T. Tulenko
The effects of low-density lipoprotein (LDL) from normolipidemic (NL) and familial hypercholesterolemic (FH) human subjects on the smooth muscle cell (SMC) proliferation were examined, along with the antiproliferative actions of heparin and glycosaminoglycans (GAGs) in this system. Cell growth was stimulated from 146 to 176% by FH-over NL-LDL. This proliferative effect of FH-LDL was accompanied by an increase in the membrane cholesterol content and an increase in Ca2+ influx. These effects of FH-LDL were partially inhibited (50%) following methylation of apoprotein B100· The effects of FH-LDL were abolished by heparin and sulfated GAGs and this inhibitory effect was also accompanied by normalization of Ca2+ influx and cell membrane cholesterol. Electrokinetic analysis demonstrated a reduced net negative charge of FH-LDL relative to that of NL-LDL. We hypothesize that LDL surface charge may regulate the movement of cholesterol into the SMC plasma membrane where its presence in excess alters SMC function. Taken together, these results implicate a role for FH-LDL cholesterol as an important factor in the alteration of SMC cell growth kinetics in hypercholesterolemia, a process which can be modulated by heparin and sulfated GAGs.
