晚期糖基化终产物刺激兔血管平滑肌细胞中的丝裂原活化蛋白激酶并促进其增殖。
Advanced glycation endproducts stimulate mitogen-activated protein kinase and proliferation in rabbit vascular smooth muscle cells.
作者信息
Satoh H, Togo M, Hara M, Miyata T, Han K, Maekawa H, Ohno M, Hashimoto Y, Kurokawa K, Watanabe T
机构信息
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
出版信息
Biochem Biophys Res Commun. 1997 Oct 9;239(1):111-5. doi: 10.1006/bbrc.1997.7424.
Advanced glycation end products of bovine serum albumin (AGEs-BSA) exhibited biphasic effects on the proliferation of cultured rabbit vascular smooth muscle cells (VSMCs) in terms of [3H]thymidine incorporation and cell number count; a stimulatory effect was observed at 1-10 micrograms/ml and an inhibitory effect at more than 20 micrograms/ml, while it inhibited [3H]thymidine incorporation even at 1-10 micrograms/ml in cultured bovine vascular endothelial cells (VECs). Transient activation of p42 mitogen-activated protein kinase (MAPK) with a peak at around 5 min and a subsequent sustained phase was induced by AGEs-BSA in VSMCs, but not in VECs. The dependence of MAPK activation on AGEs-BSA dose was correlated with that of VSMCs proliferation.
就[3H]胸腺嘧啶核苷掺入和细胞计数而言，牛血清白蛋白晚期糖基化终产物（AGEs-BSA）对培养的兔血管平滑肌细胞（VSMC）增殖呈现双相效应；在1 - 10微克/毫升时观察到刺激作用，超过20微克/毫升时则为抑制作用，而在培养的牛血管内皮细胞（VEC）中，即使在1 - 10微克/毫升时它也抑制[3H]胸腺嘧啶核苷掺入。AGEs-BSA在VSMC中诱导p42丝裂原活化蛋白激酶（MAPK）短暂激活，峰值出现在约5分钟左右，随后进入持续阶段，但在VEC中未出现这种情况。MAPK激活对AGEs-BSA剂量的依赖性与VSMC增殖的依赖性相关。
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