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Activation of MAP kinase superfamily signaling pathways by methylglyoxal

机译:甲基乙醛的MAP激酶超细信号通信途径的激活

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Highly reactive dicarbonyl compounds such as methylglyoxal (MG) form through the glycation reaction, causing so-called carbonyl stress under diabetic conditions. It has been hypothesized that MG potentially influences cell functions by itself in diabetic tissues in addition to its action as a precursor of several AGEs. We therefore investigated whether MG activated MAP kinase (MAPK) superfamily including JNK and p38 MAPK that was known to be activated in response to various cellular stresses, using primary culture of rat mesangial cells (RMC). Immunoblot analysis of RMC lysate revealed that MG induced pbosphorylation and activation of JNK. On the other hand, p38 MAPK, another member of MAPK superfamily, was also activated in RMC by the incubation with MG. These findings suggest a potential role of MG-induced activation of MAPK superfamily signaling pathways in the development of diabetic complications including nephropathy.
机译:通过糖糖反应,高反应性二羰基化合物如甲基甘油(Mg)形式,使糖尿病条件下称为所谓的羰基胁迫。已经假设,除了作为几年龄段的前体之外,Mg潜在地影响细胞功能本身在糖尿病组织中。因此,我们研究了MG活化的MAP激酶(MAPK)超家族是否包括响应于各种细胞应力而被激活的JNK和P38 MAPK,使用大鼠Mesangial细胞(RMC)的初级培养。 RMC裂解物的免疫印迹分析显示Mg诱导磷酸化和JNK的活化。另一方面,P38 MAPK是MAPK Superfamily的另一个成员,在RMC中也通过与Mg孵育来激活。这些研究结果表明MG诱导的MAPK超家族信号传导途径在糖尿病并发症的发展中的激活潜在作用。

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