Expression of monocyte chemoattractant protein-1 by nonenzymatically glycated albumin (Amadori adducts) in vascular smooth muscle cells.

Expression of monocyte chemoattractant protein-1 by nonenzymatically glycated albumin (Amadori adducts) in vascular smooth muscle cells.
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血管平滑肌细胞中非酶糖化白蛋白(阿马多里加合物)表达单核细胞趋化蛋白-1。

DOI:
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发表时间:
2000
期刊:
Biochemical and Biophysical Research Communications - BBRC
影响因子:
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通讯作者:
A. Takeshita
A. Takeshita
中科院分区:
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文献类型:
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作者:
T. Ichiki;Y. Funakoshi;K. Ito;A. Takeshita

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阿马多里加合物是早期非酶促糖化蛋白,其对血管细胞的生物学作用尚不清楚。我们检测了糖化血清白蛋白(GA)对单核细胞趋化蛋白-1(MCP-1)表达的影响,单核细胞趋化蛋白-1是一种将单核细胞募集至血管的重要趋化因子。 GA 增加了 MCP-1 mRNA 的表达,刺激 3 小时后达到峰值。 GA 对 MCP-1 的诱导具有剂量依赖性。 GA 的 MCP-1 mRNA 表达被 PD98059 和金雀异黄素完全抑制,分别抑制丝裂原激活蛋白 (MAP) 激酶激酶和酪氨酸激酶。 N-乙酰半胱氨酸是一种有效的抗氧化剂,也能抑制 GA 诱导的 MCP-1 表达。这些结果表明,GA 诱导活性氧的产生并激活 VSMC 中的酪氨酸激酶和 MAP 激酶。这些信号的激活导致 MCP-1 表达。 GA诱导的MCP-1表达可能是糖尿病患者动脉粥样硬化加速的机制之一。
The biological effects of Amadori adducts that are early nonenzymatically glycated protein on vascular cells were poorly defined. We examined the effect of glycated serum albumin (GA) on the expression of monocyte chemoattractant protein-1(MCP-1) that is an important chemokine recruiting monocyte to blood vessel. GA increased MCP-1 mRNA expression with a peak after 3 h of stimulation. The induction of MCP-1 by GA was dose-dependent. The MCP-1 mRNA expression by GA was completely inhibited by PD98059 and genistein that inhibit mitogen activated protein (MAP) kinase kinase and tyrosine kinase, respectively. N-Acetylcysteine, a potent antioxidant, also suppressed the GA-induced MCP-1 expression. These results suggest that GA induces production of reactive oxygen species and activates tyrosine kinase and MAP kinase in VSMC. Activation of these signals results in MCP-1 expression. GA-induced MCP-1 expression may be one of the mechanisms by which the diabetic patients suffer from accelerated atherosclerosis.
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发表时间: 1989
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