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首页> 外文期刊>Life sciences >Developmental changes of Ca(2+) handling in mouse ventricular cells from early embryo to adulthood.
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Developmental changes of Ca(2+) handling in mouse ventricular cells from early embryo to adulthood.

机译：从早期胚胎到成年小鼠心室细胞中Ca（2+）处理的发展变化。

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Transplant of immature cardiomyocytes is recently attracting a great deal of interest as a new experimental strategy for the treatment of failing hearts. Full understanding of normal cardiomyogenesis is essential to make this regenerative therapy feasible. We analyzed the molecular and functional changes of Ca(2+) handling proteins during development of the mouse heart from early embryo at 9.5 days postcoitum (dpc) through adulthood. From the early to the late (18 dpc) embryonic stage, mRNAs estimated by the real time PCR for ryanodine receptor (type 2, RyR2), sarcoplasmic reticulum (SR) Ca(2+) pump (type 2, SERCA2) and phospholamban (PLB) increased by 3-15 fold in the values normalized to GAPDH mRNA, although Na(+)/Ca(2+) exchanger (type 1, NCX1) mRNA was unchanged. After birth, there was a further increase in the mRNAs for RyR2, SERCA2 and PLB by 18-33 fold, but a 50% decrease in NCX1 mRNA. The protein levels of RyR2, SERCA2, PLB and NCX1, which were normalized to total protein, showed qualitatively parallel developmental changes. L-type Ca(2+) channel currents (I(Ca-L)) were increased during the development (1.3-fold at 18 dpc, 2.2-fold at adult stage, vs. 9.5 dpc). At 9.5 dpc, the Ca(2+) transient was, unlike adulthood, unaffected by the SR blockers, ryanodine (5 microM) and thapsigargin (2 microM), and also by a blocker of the Ca(2+) entry via Na(+)/Ca(2+) exchanger, KB-R 7943 (1 microM). The Ca(2+) transient was abolished after application of nisoldipine (5 microM). These results indicate that activator Ca(2+) for contraction in the early embryonic stage depends almost entirely on I(Ca-L).
机译：作为治疗心力衰竭的新实验策略，不成熟心肌细胞的移植近来引起了极大的兴趣。充分了解正常的心肌发生对于使这种再生疗法可行至关重要。我们分析了小鼠心脏发育过程中Ca（2+）的分子和功能变化，该过程从成年后9.5天（dpc）到成年的早期胚胎从早期胚胎开始。从早期到晚期（18 dpc）胚胎阶段，通过实时PCR估计的雷诺丁受体（2型，RyR2），肌质网（SR）Ca（2+）泵（2型，SERCA2）和磷酰胺（尽管Na（+）/ Ca（2+）交换子（1型，NCX1）mRNA不变，但在归一化为GAPDH mRNA的值中，PLB）增加了3-15倍。出生后，RyR2，SERCA2和PLB的mRNA进一步增加了18-33倍，但NCX1 mRNA却降低了50％。相对于总蛋白质标准化的RyR2，SERCA2，PLB和NCX1的蛋白质水平在质量上显示出平行的发育变化。 L型Ca（2+）通道电流（I（Ca-L））在开发过程中有所增加（18 dpc时为1.3倍，成人阶段为2.2倍，而9.5 dpc）。在9.5 dpc时，与成年不同，Ca（2+）瞬变不受SR阻滞剂，ryanodine（5 microM）和thapsigargin（2 microM），也不受Ca（2+）经由Na（ +）/ Ca（2+）交换器，KB-R 7943（1 microM）。应用尼索地平（5 microM）后，取消了Ca（2+）瞬变。这些结果表明，在胚胎早期阶段收缩的活化剂Ca（2+）几乎完全取决于I（Ca-L）。

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