NDLI: Muscle RING finger-1 attenuates IGF-I-dependent cardiomyocyte hypertrophy by inhibiting JNK signaling

Content Provider	PubMed Central
Author	Wadosky, Kristine M. RodrÃguez, Jessica E. Hite, Rebecca L. Min, Jin-na Walton, Bethany L. Willis, Monte S.
Copyright Year	2014
Abstract	Recent studies implicate the muscle-specific ubiquitin ligase muscle RING finger-1 (MuRF1) in inhibiting pathological cardiomyocyte growth in vivo by inhibiting the transcription factor SRF. These studies led us to hypothesize that MuRF1 similarly inhibits insulin-like growth factor-I (IGF-I)-mediated physiological cardiomyocyte growth. We identified two lines of evidence to support this hypothesis: IGF-I stimulation of cardiac-derived cells with MuRF1 knockdown 1) exhibited an exaggerated hypertrophy and, 2) conversely, increased MuRF1 expression-abolished IGF-I-dependent cardiomyocyte growth. Enhanced hypertrophy with MuRF1 knockdown was accompanied by increases in Akt-regulated gene expression. Unexpectedly, MuRF1 inhibition of this gene expression profile was not a result of differences in p-Akt. Instead, we found that MuRF1 inhibits total protein levels of Akt, GSK-3β (downstream of Akt), and mTOR while limiting c-Jun protein expression, a mechanism recently shown to govern Akt, GSK-3β, and mTOR activities and expression. These findings establish that MuRF1 inhibits IGF-I signaling by restricting c-Jun activity, a novel mechanism recently identified in the context of ischemia-reperfusion injury. Since IGF-I regulates exercise-mediated physiological cardiac growth, we challenged MuRF1−/− and MuRF1-Tg+ mice and their wild-type sibling controls to 5 wk of voluntary wheel running. MuRF1−/− cardiac growth was increased significantly over wild-type control; conversely, the enhanced exercise-induced cardiac growth was lost in MuRF1-Tg+ animals. These studies demonstrate that MuRF1-dependent attenuation of IGF-I signaling via c-Jun is applicable in vivo and establish that further understanding of this novel mechanism may be crucial in the development of therapies targeting IGF-I signaling.
Related Links	http://dx.doi.org/10.1152/ajpendo.00326.2013
Starting Page	723
File Format	PDF
ISSN	01931849
e-ISSN	15221555
Journal	American Journal of Physiology - Endocrinology and Metabolism
Issue Number	7
Volume Number	306
Language	English
Publisher	American Physiological Society
Publisher Date	2014-04-01
Access Restriction	Open
Rights Holder	American Physiological Society
Subject Keyword	Physiology (medical) Physiology Endocrinology, Diabetes and Metabolism Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Endocrinology, Diabetes and Metabolism Physiology (medical)

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