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Soluble activin receptor type IIB increases forward pulling tension in the mdx mouse
Author(s) -
George Carlson C.,
Bruemmer Kay,
Sesti Jenna,
Stefanski Casey,
Curtis Heather,
Ucran Jeffrey,
Lachey Jennifer,
Seehra Jasbir S.
Publication year - 2011
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21944
Subject(s) - myostatin , endocrinology , mdx mouse , medicine , activin receptor , receptor , chemistry , duchenne muscular dystrophy , biology , muscle hypertrophy , dystrophin
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. Muscle Nerve, 2011