title: 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.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.
authors.forename: Jian
authors.initials: J
authors.lastname: Ding
authors.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.|Department of Orthopaedic Surgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
authors.forename: Mao
authors.initials: M
authors.lastname: Nie
authors.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.
authors.forename: Jianming
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Hu
authors.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.|College of Life Sciences, Hubei University, Wuhan, Hubei, China.
authors.forename: Lixin
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Orthopaedic Surgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
authors.forename: Zhong-Liang
authors.initials: ZL
authors.lastname: Deng
authors.affiliation: Department of Cardiology, Boston Children's Hospital, Harvard Medical School, 320 Longwood Avenue, Boston, Massachusetts, United States of America.|Harvard Stem Cell Institute, Harvard University, Cambridge, Massachusetts, United States of America.
authors.forename: Da-Zhi
authors.initials: DZ
authors.lastname: Wang
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D018482:Muscle, Skeletal / Q000502:physiology*; D056918:Nuclear Receptor Coactivators / Q000235:genetics / Q000502:physiology*; D012038:Regeneration
chemical_list: C486559:NCOA6 protein, human; D056918:Nuclear Receptor Coactivators