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Articles by Z. Yan
Total Records ( 2 ) for Z. Yan
  J. M McClung , A. R Judge , S. K Powers and Z. Yan
 

Oxidative stress is a primary trigger of cachectic muscle wasting, but the signaling pathway(s) that links it to the muscle wasting processes remains to be defined. Here, we report that activation of p38 mitogen-activated protein kinase (MAPK) (phosphorylation) and increased oxidative stress (trans-4-hydroxy-2-nonenal protein modification) in skeletal muscle occur as early as 8 h after lipopolysaccharide (1 mg/kg) and 24 h after dexamethasone (25 mg/kg) injection (intraperitoneal) in mice, concurrent with upregulation of autophagy-related genes, Atg6, Atg7, and Atg12. Treating cultured C2C12 myotubes with oxidant hydrogen peroxide (4 h) resulted in increased p38 phosphorylation and reduced FoxO3 phosphorylation along with induced Atg7 mRNA expression without activation of NF-B or FoxO3a transcriptional activities. Furthermore, inhibition of p38/β by SB202190 blocked hydrogen peroxide-induced atrophy with diminished upregulation of Atg7 and atrogenes [muscle atrophy F-box protein (MAFbx/Atrogin-1), muscle ring finger protein 1 (MuRF-1), and Nedd4]. These findings provide direct evidence for p38/β MAPK in mediating oxidative stress-induced autophagy-related genes, suggesting that p38/β MAPK regulates both the ubiquitin-proteasome and the autophagy-lysosome systems in muscle wasting.

  T Geng , P Li , M Okutsu , X Yin , J Kwek , M Zhang and Z. Yan
 

Endurance exercise stimulates peroxisome proliferator-activated receptor coactivator-1 (PGC-1) expression in skeletal muscle, and forced expression of PGC-1 changes muscle metabolism and exercise capacity in mice. However, it is unclear if PGC-1 is indispensible for endurance exercise-induced metabolic and contractile adaptations in skeletal muscle. In this study, we showed that endurance exercise-induced expression of mitochondrial enzymes (cytochrome oxidase IV and cytochrome c) and increases of platelet endothelial cell adhesion molecule-1 (PECAM-1, CD31)-positive endothelial cells in skeletal muscle, but not IIb-to-IIa fiber-type transformation, were significantly attenuated in muscle-specific Pgc-1 knockout mice. Interestingly, voluntary running effectively restored the compromised mitochondrial integrity and superoxide dismutase 2 (SOD2) protein expression in skeletal muscle in Pgc-1 knockout mice. Thus, PGC-1 plays a functional role in endurance exercise-induced mitochondrial biogenesis and angiogenesis, but not IIb-to-IIa fiber-type transformation in mouse skeletal muscle, and the improvement of mitochondrial morphology and antioxidant defense in response to endurance exercise may occur independently of PGC-1 function. We conclude that PGC-1 is required for complete skeletal muscle adaptations induced by endurance exercise in mice.

 
 
 
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