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首页> 外文期刊>Circulation research: a journal of the American Heart Association >beta-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.
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beta-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.

机译：β-肌球蛋白重链是由较小的小鼠心肌细胞的较小亚群中的压力超负荷诱导的。

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RATIONALE: Induction of the fetal hypertrophic marker gene beta-myosin heavy chain (beta-MyHC) is a signature feature of pressure overload hypertrophy in rodents. beta-MyHC is assumed present in all or most enlarged myocytes. OBJECTIVE: To quantify the number and size of myocytes expressing endogenous beta-MyHC by a flow cytometry approach. METHODS AND RESULTS: Myocytes were isolated from the left ventricle of male C57BL/6J mice after transverse aortic constriction (TAC), and the fraction of cells expressing endogenous beta-MyHC was quantified by flow cytometry on 10,000 to 20,000 myocytes with use of a validated beta-MyHC antibody. Side scatter by flow cytometry in the same cells was validated as an index of myocyte size. beta-MyHC-positive myocytes constituted 3 +/- 1% of myocytes in control hearts (n=12), increasing to 25 +/- 10% at 3 days to 6 weeks after TAC (n=24, P<0.01). beta-MyHC-positive myocytes did not enlarge with TAC and were smaller at all times than myocytes without beta-MyHC ( approximately 70% as large, P<0.001). beta-MyHC-positive myocytes arose by addition of beta-MyHC to alpha-MyHC and had more total MyHC after TAC than did the hypertrophied myocytes that had alpha-MyHC only. Myocytes positive for beta-MyHC were found in discrete regions of the left ventricle in 3 patterns: perivascular, in areas with fibrosis, and in apparently normal myocardium. CONCLUSIONS: beta-MyHC protein is induced by pressure overload in a minor subpopulation of smaller cardiac myocytes. The hypertrophied myocytes after TAC have alpha-MyHC only. These data challenge the current paradigm of the fetal hypertrophic gene program and identify a new subpopulation of smaller working ventricular myocytes with more myosin.
机译：理由：胎儿肥大标记基因β-肌球蛋白重链（β-MyHC）的诱导是啮齿动物压力超负荷肥大的标志性特征。假定β-MyHC存在于所有或大多数扩大的心肌细胞中。目的：通过流式细胞仪量化表达内源性β-MyHC的心肌细胞的数量和大小。方法和结果：从雄性C57BL / 6J小鼠的主动脉横动脉收缩后（TAC）分离了心肌细胞，并通过流式细胞术对10,000至20,000个心肌细胞中表达内源性β-MyHC的细胞部分进行了定量分析。 β-MyHC抗体。通过流式细胞术在相同细胞中的侧向散射被确认为肌细胞大小的指标。 β-MyHC阳性心肌细胞占对照组心脏细胞的3 +/- 1％（n = 12），在TAC后3天至6周时增加到25 +/- 10％（n = 24，P <0.01）。 TAC不会使β-MyHC阳性的肌细胞增大，并且始终比没有β-MyHC的肌细胞小（约70％，P <0.001）。 β-MyHC阳性的心肌细胞是通过在α-MyHC中添加β-MyHC而产生的，与仅具有α-MyHC的肥大性心肌细胞相比，TAC后的MyHC总量更高。在左心室的离散区域以三种模式发现了β-MyHC阳性的心肌细胞：血管周围，纤维化区域和明显正常的心肌。结论：β-MyHC蛋白是由较小的心肌细胞的较小亚群中的压力超负荷诱导的。 TAC后肥大的心肌细胞仅具有α-MyHC。这些数据挑战了胎儿肥厚基因程序的当前范例，并确定了具有更多肌球蛋白的较小工作心室肌细胞的新亚群。

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