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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Nitric oxide facilitates cardiomyogenesis in mouse embryonic stem cells
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Nitric oxide facilitates cardiomyogenesis in mouse embryonic stem cells

机译：一氧化氮促进小鼠胚胎干细胞的心肌发生

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摘要

Stem cell therapy holds great promise for the replacement of damaged or dysfunctional myocardium. Nitric oxide (NO) has been shown to promote embryonic stem (ES) cell differentiation in other systems. We hypothesized that NO, through NO synthase gene transfer or exogenous NO exposure, would promote the differentiation of mouse ES cells into cardiomyocytes (CM). In our study, NO treatment increased both the number and the size of beating foci in embryoid body (EB) outgrowths. Within 2 weeks, 69% of the inducible NO synthase-transduced EB displayed spontaneously beating foci, as did 45% of the NO donor-treated EB, compared with only approximate to15% in controls. Cardiac-specific genes and protein expression were significantly increased in NO-treated ES. Electron microscopy and immunocytochemistry revealed that these NO-induced contracting cells exhibited characteristics consistent with CM. At day 7 in culture, troponin T was expressed in 45.6 +/- 20.6% of the NO-treated ES cells but in only 9.25 +/- 1.77% of control cells. Interestingly, 50.4 +/- 18.4% of NO-treated ES cells were troponin T-negative and annexin V-positive. This apoptotic phenotype was seen in <1 % of the control ES cells. These data strongly support our hypothesis that mouse ES cells can be accelerated to differentiate into CM by NO treatment. NO may influence cardiac differentiation by both inducing a switch toward a cardiac phenotype and inducing apoptosis in cells not committed to cardiac differentiation.
机译：干细胞疗法有望替代受损或功能异常的心肌。一氧化氮（NO）已显示在其他系统中可促进胚胎干（ES）细胞分化。我们假设NO，通过NO合酶基因转移或外源NO暴露，将促进小鼠ES细胞向心肌细胞（CM）的分化。在我们的研究中，NO处理增加了胚状体（EB）增生中跳动灶的数量和大小。在2周内，69％的可诱导NO合酶转导的EB表现出自发搏动灶，NO供体治疗的EB表现为45％，而对照中只有约15％。 NO处理的ES患者的心脏特异性基因和蛋白质表达显着增加。电子显微镜和免疫细胞化学显示，这些NO诱导的收缩细胞表现出与CM一致的特征。在培养的第7天，肌钙蛋白T在45.6 +/- 20.6％的经NO处理的ES细胞中表达，但仅在对照细胞的9.25 +/- 1.77％中表达。有趣的是，NO处理的ES细胞中50.4 +/- 18.4％是肌钙蛋白T阴性和膜联蛋白V阳性。在＜1％的对照ES细胞中观察到这种凋亡表型。这些数据有力地支持了我们的假设：通过NO处理，小鼠ES细胞可以加速分化为CM。 NO可能通过诱导向心脏表型的转换和诱导未致力于心脏分化的细胞的凋亡而影响心脏分化。

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