International Journal Of Bilogical Sciences
.: Home > International Journal Of Bilogical Sciences > 2016 > Volume 12 Number 10 > Yonghui Yu*, Xiao Li*, Lingying Liu*, Jiake Chai, Zhang Haijun, Wanli Chu, Huinan Yin, Li Ma, Hongjie Duan, Mengjing Xiao
miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1
Yonghui Yu*, Xiao Li*, Lingying Liu*, Jiake Chai, Zhang Haijun, Wanli Chu, Huinan Yin, Li Ma, Hongjie Duan, Mengjing Xiao
Department of Burn & Plastic Surgery, the First Affiliated Hospital of PLA General Hospital, Beijing, 100048 China. *These authors contributed equally to this work. Corresponding author: Chai Jiake, Ph.D. Department of Burn & Plastic Surgery, the First Affiliated Hospital of PLA General Hospital, 51 Fucheng Road, Haidian District, Beijing, 100048 China. Tel: +86-10-66867972 Fax: +86-10-68989181 Email: firstname.lastname@example.org.
Skeletal muscle atrophy is a common clinical feature among patients with severe burns. Previous studies have shown that miRNAs play critical roles in the regulation of stress-induced skeletal muscle atrophy. Our previous study showed that burn-induced skeletal muscle atrophy is mediated by miR-628. In this study, compared with sham rats, rats subjected to burn injury exhibited skeletal muscle atrophy, as well as significantly decreased insulin receptor substrate 1 (IRS1) protein expression and significantly increased skeletal muscle cell apoptosis. An miRNA array showed that the levels of miR-628, a potential regulator of IRS1 protein translation, were also clearly elevated. Second, L6 myocyte cell apoptosis increased after induction of miR-628 expression, and IRS1 and p-Akt protein expression decreased significantly. Expression of the cell apoptosis-related proteins FoxO3a and cleaved caspase 3 also increased after induction of miR-628 expression. Finally, forced miR-628 expression in normal rats resulted in increased cell apoptosis and skeletal muscle atrophy, as well as changes in IRS1/Akt/FoxO3a signaling pathway activity consistent with the changes in protein expression described above. Inhibiting cell apoptosis with Z-VAD-FMK resulted in alleviation of burn-induced skeletal muscle atrophy. In general, our results indicate that miR-628 mediates burn-induced skeletal muscle atrophy by regulating the IRS1/Akt/FoxO3a signaling pathway.
miR-628; Burn; IRS1; Skeletal muscle atrophy.
Date Deposited : 07 Nov 2016 20:37
Official URL: http://www.ijbs.com/v12i10
Last Modified : 07 Nov 2016 20:37
Volume 12, Number 10, September 2016
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