Altered bone-regulating myokine expression in skeletal muscle Of Duchenne muscular dystrophy mouse models.
- Resource Type
- journal article
- Authors
- Zhou, Shumin; Qian, Baoli; Wang, Ling; Zhang, Changqing; Hogan, Macalus V.; Li, Hongshuai
- Source
- Muscle & Nerve. Oct2018, Vol. 58 Issue 4, p573-582. 10p.
- Subject
- *BONE metabolism
*RNA metabolism
*ANIMAL experimentation
*BIOLOGICAL models
*BONES
*CELL adhesion molecules
*COMPARATIVE studies
*COMPUTED tomography
*CYTOKINES
*DUCHENNE muscular dystrophy
*FEMUR
*FIBRONECTINS
*GLYCOPROTEINS
*GROWTH factors
*INTERLEUKINS
*LEG
*LUMBAR vertebrae
*RESEARCH methodology
*MEDICAL cooperation
*MEMBRANE proteins
*MICE
*OSTEOPENIA
*POLYMERASE chain reaction
*RESEARCH
*RESEARCH funding
*WESTERN immunoblotting
*EVALUATION research
*CASE-control method
*REVERSE transcriptase polymerase chain reaction
*SKELETAL muscle
- Language
- ISSN
- 0148-639X
Introduction: Duchenne muscular dystrophy (DMD) has been well characterized as a disease that affects both skeletal muscle and bone. The pathophysiology responsible for the deficits in bone tissue is still unclear.Methods: Quantitative reverse-transcription polymerase chain reaction and Western blot analyses of known myokines from skeletal muscle were performed on dystrophic mouse models and wild-type (WT) controls to identify differentially expressed bone-regulating myokines.Results: Twenty-four of 43 myokine genes demonstrated significantly different mRNA expression in the skeletal muscles of dystrophic mice when compared with muscles of WT mice. Several differently expressed bone-regulating myokine genes were identified, and their protein levels were also verified by Western blot.Conclusions: Dystrophic skeletal muscle demonstrated a significantly altered myokine gene expression profile. mRNA and protein levels of several bone-regulating myokines were significantly altered in dystrophic skeletal muscle, which suggests pathological role of bone-regulating myokines on bone homeostasis in DMD. Muscle Nerve 58: 573-582, 2018. [ABSTRACT FROM AUTHOR]