程伟, 肖颖彬. 快速起搏心房肌细胞中MAPKs表达的变化[J]. 心脏杂志, 2009, 21(3): 300-303.
    引用本文: 程伟, 肖颖彬. 快速起搏心房肌细胞中MAPKs表达的变化[J]. 心脏杂志, 2009, 21(3): 300-303.
    Expressions of MAPKs in rapidly paced atrial myocytes[J]. Chinese Heart Journal, 2009, 21(3): 300-303.
    Citation: Expressions of MAPKs in rapidly paced atrial myocytes[J]. Chinese Heart Journal, 2009, 21(3): 300-303.

    快速起搏心房肌细胞中MAPKs表达的变化

    Expressions of MAPKs in rapidly paced atrial myocytes

    • 摘要: 目的 研究快速起搏后心房肌细胞超微结构和丝裂原激活蛋白激酶(MAPKs)表达的变化。方法 原代培养大鼠的心房肌细胞,并建立快速起搏细胞模型。实验分为对照组和快速起搏组,采用Western-blot检测细胞外信号调节激酶(ERK)和p38MAPK的蛋白表达及其磷酸化水平的变化;用透射电镜观察快速起搏24 h后心房肌细胞超微结构的变化。结果 快速起搏24 h后,ERK和磷酸化ERK的表达均较起搏前明显升高(P<0.01);p38MAPK在快速起搏前后的表达无明显变化,而磷酸化p38MAPK的表达则较起搏前明显升高(P<0.01)。经过24 h的快速起搏,心房肌细胞出现糖原聚集、核固缩、空泡样变以及肌浆网扩张、线粒体肿胀、部分线粒体嵴轻度溶解等超微结构的改变。结论 快速起搏早期,原代培养的心房肌细胞超微结构发生了明显改变,同时ERK和p38MAPK被激活,这可能是心房纤颤早期心房肌细胞结构重建发生的重要机制。

       

      Abstract: AIM To study the changes of ultramicrostructure in atrial myocytes and the expressions of mitogen-activated protein kinases (MAPKs) after rapid pacing. METHODS Rat primary atrial myocytes were cultured and a rapidly paced cell model was established. The atrial myocytes were divided into rapid pacing group and control group. Western blot was employed to detect the changes of protein expressions of extra-cellular signal regulation kinase (ERK), p38MAPK and their phosphorylation level, respectively. The ultramicrostructure in atrial myocytes was observed under transmission electromicroscope at 24 hours after rapid pacing. RESULTS Expressions of ERK, p-ERK and p-p38MAPK were all upregulated at 24 hours after rapid pacing, compared to those before pacing (P<0.01), however, no significant change was observed in the expression of p38MAPK. The ultramicrostructure in atrial myocytes displayed glycogen aggregation, karyopycnosis, sarcoplasmic reticulum distention and chondriosome swelling at 24 hours after rapid pacing. CONCLUSION Obvious change of ultramicrostructure in primarily atrial myocytes takes place in the early phase of rapid pacing and at the same time ERK and p38MAPK are activated. It may be an important mechanism of structure remodeling of atrial myocytes in the early of atrial fibrillation.

       

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