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Title 

Peroxiredoxin 3 has a crucial role in the contractile function of skeletal muscle by regulating mitochondrial homeostasis

 

Prx3 에 의한 미토콘드리아 항상성 조절을 통한 근육 기능

Authors 

Kwang-Pyo LeeYeo-Jin ShinS C ChoSeung Min LeeYeong Jae BanJi Young KimEun Soo KwonDo Yeun JeongS C ParkS G RheeH A WooKi Sun Kwon

Publisher 

Elsevier

Issue Date 

2014

Citation 

Free Radical Biology and Medicine, vol. 77, no. 0, pp. 298-306

Keywords 

FatigueFree radicalsMitochondriaMitofusinMyoblastMyogenesisOxidative stressPeroxiredoxin 3Reactive oxygen speciesSkeletal muscle

Abstract 

Antioxidant systems against reactive oxygen species (ROS) are important factors in regulating homeostasis in various cells, tissues, and organs. Although ROS are known to cause to muscular disorders, the effects of mitochondrial ROS in muscle physiology have not been fully understood. Here, we investigated the effects of ROS on muscle mass and function using mice deficient in peroxiredoxin 3 (Prx3), which is a mitochondrial antioxidant protein. Ablation of Prx3 deregulated the mitochondrial network and membrane potential of myotubes, in which ROS levels were increased. We showed that the DNA content of mitochondria and ATP production were also reduced in Prx3-KO muscle. Of note, the mitofusin 1 and 2 protein levels decreased in Prx3-KO muscle, a biochemical evidence of impaired mitochondrial fusion. Contractile dysfunction was examined by measuring isometric forces of isolated extensor digitorum longus (EDL) and soleus muscles. Maximum absolute forces in both the EDL and the soleus muscles were not significantly affected in Prx3-KO mice. However, fatigue trials revealed that the decrease in relative force was greater and more rapid in soleus from Prx3-KO compared to wild-type mice. Taken together, these results suggest that Prx3 plays a crucial role in mitochondrial homeostasis and thereby controls the contractile functions of skeletal muscle.

ISSN 

0891-5849

Link 

http://dx.doi.org/10.1016/j.freeradbiomed.2014.09.010.

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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