Expression of mitochondrial regulatory genes parallels respiratory capacity and contractile function in a rat model of hypoxia-induced right ventricular hypertrophy.
Expression of mitochondrial regulatory genes parallels respiratory capacity and contractile function in a rat model of hypoxia-induced right ventricular hypertrophy.
复制标题
在缺氧诱导的右心室肥大的大鼠模型中，线粒体调节基因的表达与呼吸能力和收缩功能平行。
DOI：
10.1007/s11010-008-9867-5
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发表时间：
2008
影响因子：
4.3
通讯作者：
Essop,MFaadiel
中科院分区：
文献类型：
--
作者：
Zungu,Makhosazane;Young,MartinE;Stanley,WilliamC;Essop,MFaadiel
慢性低压低氧(CHH)增加了右心室(RV)的负荷，导致右室肥大。我们假设CHH引起不同的反应，即肥厚的RV，与左心室(LV)不同，表现为线粒体呼吸和收缩功能增强。Wistar大鼠暴露于CHH(11%O2)4周，对照组为常氧对照组。RV/体重比增加(P<；比对照组增加0.001)，而RV收缩压和发展压更高。然而，左心室收缩压和发展压显著降低。肥厚的RV持续消耗线粒体O2，ADP/O增加(与对照组相比P<；P<0.01)，质子泄漏显著减少。相反，LV线粒体O2消耗减少(P<；与对照组相比P<；<0.05)，质子泄漏显著增加。同时，线粒体调节剂在肥厚的右室表达上调，但在左室不表达。我们的数据显示，肥厚的RV诱导线粒体调节基因的表达，将呼吸能力和增强的效率与持续收缩功能联系起来。
Chronic hypobaric hypoxia (CHH) increases load on the right ventricle (RV) resulting in RV hypertrophy. We hypothesized that CHH elicits distinct responses, i.e., the hypertrophied RV, unlike the left ventricle (LV), displaying enhanced mitochondrial respiratory and contractile function. Wistar rats were exposed to 4 weeks CHH (11% O2) versus normoxic controls. RV/body weight ratio increased (P< 0.001 vs. control) while RV systolic and developed pressures were higher. However, LV systolic and developed pressures were significantly reduced. Mitochondrial O2consumption was sustained in the hypertrophied RV, ADP/O increased (P< 0.01 vs. control) and proton leak significantly decreased. Conversely, LV mitochondrial O2consumption was attenuated (P< 0.05 vs. control) and proton leak significantly increased. In parallel, expression of mitochondrial regulators was upregulated in the hypertrophied RV but not the LV. Our data show that the hypertrophied RV induces expression of mitochondrial regulatory genes linking respiratory capacity and enhanced efficiency to sustained contractile function.