新基因C10orf97参与压力超负荷性心肌肥厚

目的检测新基因C10orf97是否参与压力超负荷型心肌肥厚病程。方法通过缩窄大鼠胸主动脉横支构建压力超负荷诱导的心肌肥厚模型,在缩窄手术后的连续时间点应用血流动力学检测评价心室重构和心功能,应用实时荧光定量PCR法检测心肌肥厚标志基因心房利钠肽和C10orf97的mRNA表达。结果主动脉缩窄手术后,大鼠心脏显著肥厚,心脏体重比逐渐增加,心功能先受损后代偿性增强。心房利钠肽表达显著上调,在缩窄后第15天升高为假手术组40倍。C10orf97基因的表达在缩窄后第2天即显著上调为假手术组的2倍,在第4天降低,随后逐渐上升,第15天时表达量升高为假手术组的3倍。结论C10orf97基因参与了压力超负荷引起的心肌肥厚病程。

Novel Gene C10orf97 Involved in Pressure-overload Induced Cardiac Hypertrophy

Objective To investigate whether the novel gene C10orf97 is involved in pressure-overload induced cardiac hypertrophy. Methods Sprague-Dawley rats were operated by transverse aorta constriction （TAC） to make cardiac hypertrophy models. Left ventricular remodeling and function were evaluated by hemodynamic measurements. The mRNA expression of atrial natriuretic peptide （ANF） and C10orf97 were determined by quantitative real-time PCR. Results The left ventricular function impaired immediately, but imp.roved gradually at the seventh day and fifteenth day after the TAC surgery. The expression of ANF was greatly up-regulated during the progress.C10orf97 was significantly induced at the 2nd day of pressure overload （2 fold）. Although the expression of C10orf97 decreased at the 4th day, it continuously increased up to 3 fold at the 15th day after TAC. Conclusion Our results indicate that C10orf97 is involved in pressure-overload induced cardiac hypertrophy.