Trbp Is Required for Differentiation of Myoblasts and Normal Regeneration of Skeletal Muscle.

Abstract

Global inactivation of Trbp, a regulator of miRNA pathways, resulted in developmental defects and postnatal lethality in mice. Recently, we showed that cardiac-specific deletion of Trbp caused heart failure. However, its functional role(s) in skeletal muscle has not been characterized. Using a conditional knockout model, we generated mice lacking Trbp in the skeletal muscle. Unexpectedly, skeletal muscle specific Trbp mutant mice appear to be phenotypically normal under normal physiological conditions. However, these mice exhibited impaired muscle regeneration and increased fibrosis in response to cardiotoxin-induced muscle injury, suggesting that Trbp is required for muscle repair. Using cultured myoblast cells we further showed that inhibition of Trbp repressed myoblast differentiation in vitro. The impaired myogenesis is associated with reduced expression of muscle-specific miRNAs, miR-1a and miR-133a. Together, our study demonstrated that Trbp participates in the regulation of muscle differentiation and regeneration.

• Authors: Jian Ding, Mao Nie, Jianming Liu, Xiaoyun Hu, Lixin Ma, Zhong-Liang Deng, Da-Zhi Wang
• Journal: PloS one (PLoS One) Vol. 11 Issue 5 Pg. e0155349 ( 2016) ISSN: 1932-6203 [Electronic] United States
• PMID: 27159388 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• NCOA6 protein, human
• Nuclear Receptor Coactivators

Topics

• Animals
• Cell Differentiation (physiology)
• Mice
• Mice, Knockout
• Muscle, Skeletal (physiology)
• Nuclear Receptor Coactivators (genetics, physiology)
• Regeneration