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首页> 外文期刊>Skeletal Muscle >Expression of MuRF1 or MuRF2 is essential for the induction of skeletal muscle atrophy and dysfunction in a murine pulmonary hypertension model
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Expression of MuRF1 or MuRF2 is essential for the induction of skeletal muscle atrophy and dysfunction in a murine pulmonary hypertension model

机译：Murf1或Murf2的表达对于鼠肺动脉高压模型中骨骼肌萎缩和功能障碍的诱导至关重要

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BackgroundPulmonary hypertension leads to right ventricular heart failure and ultimately to cardiac cachexia. Cardiac cachexia induces skeletal muscles atrophy and contractile dysfunction. MAFbx and MuRF1 are two key proteins that have been implicated in chronic muscle atrophy of several wasting states.MethodsMonocrotaline (MCT) was injected over eight weeks into mice to establish pulmonary hypertension as a murine model for cardiac cachexia. The effects on skeletal muscle atrophy, myofiber force, and selected muscle proteins were evaluated in wild-type (WT), MuRF1, and MuRF2-KO mice by determining muscle weights, in vitro muscle force and enzyme activities in soleus and tibialis anterior (TA) muscle.ResultsIn WT, MCT treatment induced wasting of soleus and TA mass, loss of myofiber force, and depletion of citrate synthase (CS), creatine kinase (CK), and malate dehydrogenase (MDH) (all key metabolic enzymes). This suggests that the murine MCT model is useful to mimic peripheral myopathies as found in human cardiac cachexia. In MuRF1 and MuRF2-KO mice, soleus and TA muscles were protected from atrophy, contractile dysfunction, while metabolic enzymes were not lowered in MuRF1 or MuRF2-KO mice. Furthermore, MuRF2 expression was lower in MuRF1KO mice when compared to C57BL/6 mice.ConclusionsIn addition to MuRF1, inactivation of MuRF2 also provides a potent protection from peripheral myopathy in cardiac cachexia. The protection of metabolic enzymes in both MuRF1KO and MuRF2KO mice as well as the dependence of MuRF2 expression on MuRF1 suggests intimate relationships between MuRF1 and MuRF2 during muscle atrophy signaling.
机译：BroughtPulmonary高血压导致右心室心脏衰竭，最终达到心脏恶毒症。心脏病患者诱导骨骼肌萎缩和收缩功能障碍。 MAFBX和Murf1是两种关键蛋白质，其含有几种浪费状态的慢性肌肉萎缩。将甲胺醛（MCT）注射到小鼠中以超过肺动脉高压为心脏恶病毒的小鼠模型。通过在野生型（WT），Murf1和Murf2-Ko小鼠中，通过确定肌肉重量，体外肌肉力和胫骨前肌肉（TA ）Muscle.Resultsin wt，MCT治疗诱导毒品丧失单独和TA质量，肌纤维力丧失，氟酸盐合酶（Cs），肌酸激酶（CK）和苹果酸脱氢酶（MDH）的耗尽，并脱氢（所有关键代谢酶）。这表明鼠MCT模型可用于模仿人体心脏恶病虫病中的外周性肌病。在Murf1和Murf2-Ko小鼠中，Soleus和Ta肌肉受到萎缩，收缩功能障碍，而Murf1或Murf2-Ko小鼠的代谢酶没有降低。此外，与C57BL / 6小鼠相比Murf1KO小鼠Murf2表达较低。结合Murf1的组合，Murf2的灭活还提供了在心脏病症中的外周肌病的有效保护。 Murf1ko和Murf2Ko小鼠中的代谢酶的保护以及Murf2在Murf1上的依赖性表明Murf1和Murf2之间的亲密关系在肌肉萎缩信号中。

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