The role of Candiotrophin-1 and its receptoi component, rpbi, in the heart.

心肌营养因子-1 （Cardiotrophin-1, CT-1）是一种有效的细胞因子，它通过gp130信号传导刺激心肌细胞中肌合成单位的串联组装，导致心肌细胞肥大。我们检测了CT-1和gp130系统在两种充血性心力衰竭大鼠模型中的作用。目的：阐明CT-1和gp130信号通路在心肌梗死后心室重构中的作用。我们检测了CT-1和gp130在大鼠心肌梗死模型中的表达。超声心动图证实所有动物均出现大面积心肌梗死、进行性左心室扩张和存活心肌肥厚不足。采用半定量RT-PCR和Southern印迹法检测CT-1和gp130 mRNA水平。结果显示，与假手术大鼠相比，假手术大鼠在梗死后1、3、7、14、28和56天的梗死区、室间隔和右心室的CT-1和gp130 mRNA水平显著升高。Western blot检测CT-和gp130蛋白水平均较假手术大鼠显著升高，在上述三个区域均在急性期达到峰值，随后下降。免疫组化染色显示，心肌细胞和成纤维细胞样细胞中检测到CT-1和gp130的免疫反应，梗死后7d染色强度较假手术大鼠增加。因此，增强的CT-1和gp130系统似乎在心肌梗死后心室重构中起重要作用。我们还用dah1 -盐敏感的高血压大鼠测定了从心脏肥厚到心力衰竭转变过程中CT-1和gp130的表达水平。CT-1表达在心力衰竭阶段增加，我们证实了肌共聚单位的串联组装。因此，CT-1通过延长心肌细胞来促进心室扩张。这些在两种心力衰竭模型中的发现强烈表明，CT-1在心力衰竭的心室扩张中起着核心作用。少

Cardiotrophin-1 (CT-1) is a potent cytokine that stimulates the assembly of sarcomeric units in series in cardiomyocytes through gp130 signaling, resulting in myocardial cell hypertrophy. We examined the role of CT-1 and gp130 system in the two rat models of congestive heart failure. TO clarify the role of CT-1 and the gp130-signaling pathway during ventricular remodeling after myocardial infarction. we examined the expression of CT-1 and gp130 in a rat model of myocardial infarction. All animals developed large myocardial infarctions and progressive left ventricular dilatation and inadequate hypertrophy of the surviving myocardium were confirmed by echocardiography. CT-1 and gp130 mRNA levels were determined by semiquantitative RT-PCR followed by Southern blotting. The densitometric analysis of the Southern blots revealed a significant increase in CT-1 and gp130 mRNA levels compared with those of the sham-operated rats at 1, 3, 7, 14, 28 and 56 days post-infarct in the infarct area, t … More he ventricular septum and right ventricle. The protein levels of CT- and gp130, determined by Western blot analysis, were significantly increased compared to those of sham-operated rats, and peaked in the acute stage and declined thereafter in the three regions described above. Immunohistochemical staining showed that CT-1 and gp130-immunoreactivities were detected in cardiomyocytes and fibroblast-like cells and that the intensity of staining was increased at 7days post-infarct compared with that in sham-operated rats. An augmented CT-1 and gp130 system thus seems to play an important role during ventricular remodeling after myocardial infarction. We also determined the expression levels of CT-1 and gp130 during the transition from cardiac hypertrophy to heart failure using Dah1-salt-sensitive rats with hypertension. CT-1 expression was increased in the stage of heart failure, in which we confirmed the assembly of sarcomeric units in series. Thus, CT-1 contributes to the ventricular dilatation by elongating cardiomyocytes. These findings in the two heart failure models strongly suggest that CT-1 plays a central role in the ventricular dilatation in heart failure. Less