Chen J K, Hoshi H, McKeehan W L
W. Alton Jones Cell Science Center, Inc., Lake Placid, New York 12946.
In Vitro Cell Dev Biol. 1988 Mar;24(3):199-204. doi: 10.1007/BF02623547.
Purified heparin-binding growth factor-1 (HBGF-1) stimulated low density lipoprotein binding, internalization, and degradation in isolated human adult arterial smooth muscle cells. Exposure of quiescent cells to HBGF-1 in serum-free, defined medium increased both low density lipoprotein (LDL) receptor activity and de novo cholesterol biosynthesis. Both events preceded the onset of DNA synthesis by 6 to 9 h. HBGF-1 acted additively with platelet-derived growth factor (PDGF) to maximally stimulate cell surface LDL receptor binding activity and DNA synthesis in the smooth muscle cells. The presence of LDL was required for maximal mitogenic activity of HBGF-1 and PDGF. In the presence of LDL, growth factor-stimulated, proliferating human smooth muscle cells accumulated cholesterol ester and triglycerides. The results suggest that HBGF-1, PDGF, and LDL act together to promote the maximal proliferation of smooth muscle cells in culture. Chronic exposure to the three growth promoters may contribute to the smooth muscle cell hyperplasia and lipid accumulation observed in atherosclerotic lesions.
纯化的肝素结合生长因子-1（HBGF-1）可刺激分离的成人人类动脉平滑肌细胞中的低密度脂蛋白结合、内化及降解。在无血清、特定培养基中，将静止细胞暴露于HBGF-1可增加低密度脂蛋白（LDL）受体活性及从头胆固醇生物合成。这两个事件均先于DNA合成6至9小时发生。HBGF-1与血小板衍生生长因子（PDGF）协同作用，最大程度地刺激平滑肌细胞表面LDL受体结合活性及DNA合成。HBGF-1和PDGF的最大促有丝分裂活性需要LDL的存在。在LDL存在的情况下，生长因子刺激的增殖性人类平滑肌细胞会积累胆固醇酯和甘油三酯。结果表明，HBGF-1、PDGF和LDL共同作用，以促进培养的平滑肌细胞的最大增殖。长期暴露于这三种生长促进剂可能导致动脉粥样硬化病变中观察到的平滑肌细胞增生和脂质积累。
