Published online before print February 1, 2007, doi: 10.1161/01.RES.0000259559.48597.32
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Submitted on December 13, 2006
Revised on January 17, 2007
Accepted on January 23, 2007
Muscle Ring Finger 1, but not Muscle Ring Finger 2, Regulates Cardiac Hypertrophy In Vivo
Monte S. Willis ;
From the Carolina Cardiovascular Biology Center (M.S.W., C.I., D.-Z.W., C.P.), Department of Pathology and Laboratory Medicine (M.S.W., L.L.), Department of Cell and Developmental Biology (D.-Z.W., C.P), University of North Carolina, Chapel Hill, NC; Regeneron Pharmaceuticals (D.J.G.), Tarrytown, NY.
* To whom correspondence should be addressed. E-mail: cpatters{at}med.unc.edu.
Muscle ring finger (MuRF) proteins have been implicated in transmitting mechanical forces to cell signaling pathways through their interactions with the giant protein titin. Recent evidence has linked mechanically-induced stimuli with the control of serum response factor activity and localization through MuRF2. This observation is particularly intriguing in the context of cardiac hypertrophy, where serum response factor transactivation is a key event necessary for the induction of cardiac hypertrophy in response to increased afterload. We have previously reported that MuRF1, which is also a titin-associated protein, exerts antihypertrophic activity in vitro. In the present study, we induced cardiac hypertrophy in mice lacking MuRF1 and MuRF2 to distinguish the physiologic role of these divergent proteins in vivo. We identified for the first time that MuRF1, but not MuRF2, plays a key role in regulating the induction of cardiac hypertrophy, likely by its direct interactions with serum response factor. These studies describe for the first time distinct and nonoverlapping functional characteristics of MuRF1 and MuRF2 in response to cardiac stress in vivo.
Key words: adenosine receptors • heat shock proteins • proteasome • serum response factor • ubiquitin
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