B-GPA administration activates slow oxidative muscle signaling pathways and protects soleus muscle against the increased fatigue under 7-days of rat hindlimb suspension

被引:2
|
作者
Sharlo, K. A. [1 ]
Lvova, I. D. [1 ]
Sidorenko, D. A. [1 ]
Tyganov, S. A. [1 ]
Sharlo, D. T. [2 ]
Shenkman, B. S. [1 ]
机构
[1] Inst Biomed Problems RAS, Myol Lab, Moscow, Russia
[2] Bauman Moscow State Tech Univ, Fed State Budgetary Educ Inst Higher Educ, Moscow, Russia
关键词
SKELETAL-MUSCLE; EXPRESSION; FATIGABILITY; IMMOBILIZATION; ADAPTATIONS; METABOLISM; ISOFORM;
D O I
10.1016/j.abb.2023.109647
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Unloading of slow-twitch muscles results in increased muscle fatigue and the mechanisms of this effect are poorly studied. We aimed to analyze the role of high-energy phosphates accumulation during the first week of rat hindlimb suspension plays in a fiber-type phenotype shift towards fast-type fatigable muscle fibers. Male Wistar rats were divided into 3 groups (n = 8): C -vivarium control; 7HS -7-day hindlimb suspension; 7HB -7-day hindlimb suspension with intraperitoneal injection of beta-guanidine propionic acid (8-GPA, 400 mg/kg b w). 8-GPA is a competitive inhibitor of creatine kinase and it reduces concentrations of ATP and phosphocreatine. In the 7HB group, 8-GPA treatment protected a slow-type signaling network in an unloaded soleus muscle, including MOTS-C, AMPK, PGC1 alpha and micro-RNA-499. These signaling effects resulted in a preserved soleus muscle fatigue resistance, slow-type muscle fibers percentage and mitochondrial DNA copy number under muscle unloading.
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页数:10
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