Soluble activin receptor type IIB increases forward pulling tension in the mdx mouse

Source

Department of Physiology, Kirksville College Osteopathic Medicine, AT Still University, Kirksville, Missouri 63501, USA. ccarlson@atsu.edu

Abstract

INTRODUCTION:

In this study we investigated the action of RAP-031, a soluble activin receptor type IIB (ActRIIB) comprised of a form of the ActRIIB extracellular domain linked to a murine Fc, and the NF-κB inhibitor, ursodeoxycholic acid (UDCA), on the whole body strength of mdx mice.

METHODS:

The whole body tension (WBT) method of assessing the forward pulling tension (FPT) exerted by dystrophic (mdx) mice was used.

RESULTS:

RAP-031 produced a 41% increase in body mass and a 42.5% increase in FPT without altering the FPT normalized for body mass (WBT). Coadministration of RAP-031 with UDCA produced increases in FPT that were associated with an increase in WBT.

CONCLUSIONS:

Myostatin inhibition increases muscle mass without altering the fundamental weakness characteristic of dystrophic muscle. Cotreatment with an NF-κB inhibitor potentiates the effects of myostatin inhibition in improving FPT in mdx mice.

Copyright © 2011 Wiley Periodicals, Inc.

PMID:
21462203
[PubMed – indexed for MEDLINE]
PMCID: PMC3075386
[Available on 2012/5/1]

Myostatin: a novel insight into its role in metabolism, signal pathways, and expression regulation.

Source

Institute of Animal Nutrition, Sichuan Agricultural University, Yaan, Sichuan 625014, PR China.

Abstract

Myostatin, a member of the transforming growth factor-β (TGF-β) superfamily, is a critical autocrine/paracrine inhibitor of skeletal muscle growth. Since the first observed double-muscling phenotype was reported in myostatin-null animals, a functional role of myostatin has been demonstrated in the control of skeletal muscle development. However, beyond the confines of its traditional role in muscle growth inhibition, myostatin has recently been shown to play an important role in metabolism. During the past several years, it has been well established that Smads are canonical mediators of signals for myostatin from the receptors to the nucleus. However, growing evidence supports the notion that Non-Smad signal pathways also participate in myostatin signaling. Myostatin expression is increased in muscle atrophy and metabolic disorders, suggesting that changes in endogenous expression of myostatin may provide therapeutic benefit for these diseases. MicroRNAs (miRNAs) are a class of non-coding RNAs that negatively regulate gene expression and recent evidence has accumulated supporting a role for miRNAs in the regulation of myostatin expression. This review highlights some of these areas in myostatin research: a novel role in metabolism, signal pathways, and miRNA-mediated expression regulation.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID:
21609762
[PubMed – in process]
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