Antibodies against a putative heparin receptor slow cell proliferation and decrease MAPK activation in vascular smooth muscle cells.
Antibodies against a putative heparin receptor slow cell proliferation and decrease MAPK activation in vascular smooth muscle cells.
复制标题
针对假定的肝素受体的抗体可减缓细胞增殖并减少血管平滑肌细胞中的 MAPK 激活。
DOI：
10.1002/jcp.1076
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发表时间：
2001
影响因子：
5.6
通讯作者：
Lowe-Krentz,LJ
中科院分区：
文献类型：
--
作者：
Savage,JM;Gilotti,AC;Granzow,CA;Molina,F;Lowe-Krentz,LJ
肝素长期以来被认为可以减缓血管平滑肌细胞的生长。然而，肝素作用的机制尚未解决。用阻断肝素与细胞结合的抗体鉴定内皮细胞中假定的肝素受体提供了进一步检查肝素受体可能参与平滑肌细胞对肝素的反应的手段。平滑肌细胞蛋白与抗肝素受体抗体的免疫沉淀提供了该蛋白存在于平滑肌细胞中的证据。使用抗肝素受体抗体的实验表明，抗体可以模拟肝素降低PDGF诱导的胸苷和BrdU掺入。还发现抗肝素受体抗体在活化后与肝素类似地降低MAPK活性水平。这些结果支持肝素受体的鉴定及其在肝素对血管平滑肌细胞生长的影响中的作用。© 2001 Wiley利斯公司
Heparin has long been known to slow the growth of vascular smooth muscle cells. However, the mechanism(s) by which heparin acts has yet to be resolved. The identification of a putative heparin receptor in endothelial cells with antibodies that blocked heparin binding to the cells provided the means to further examine the possible involvement of a heparin receptor in smooth muscle cell responses to heparin. Immunoprecipitation of a smooth muscle cell protein with the anti‐heparin receptor antibodies provided evidence that the protein was present in smooth muscle cells. Experiments with the anti‐heparin receptor antibodies indicate that the antibodies can mimic heparin in decreasing PDGF induced thymidine and BrdU incorporation. The anti‐heparin receptor antibodies were also found to decrease MAPK activity levels after activation similarly to heparin. These results support the identification of a heparin receptor and its role in heparin effects on vascular smooth muscle cell growth. © 2001 Wiley‐Liss, Inc.