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3‐hydroxy 3‐methylglutaryl coenzyme A reductase increase is essential for rat muscle differentiation
Author(s) -
Martini Chiara,
Trapani Laura,
Narciso Laura,
Marino Maria,
Trentalance Anna,
Pallottini Valentina
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21810
Subject(s) - myocyte , hmg coa reductase , regulator , biology , microbiology and biotechnology , reductase , endocrinology , medicine , pharmacology , enzyme , biochemistry , gene
Abstract 3‐Hydroxy 3‐methylglutaryl coenzyme A reductase (HMG‐CoAR) is the key and rate‐limiting enzyme of cholesterol biosynthetic pathway. Although HMG‐CoAR activity has already been related to the differentiation of some cellular lines there are no studies that analyze the role of HMG‐CoAR, and the pathway it is involved with in a fully characterized muscle differentiation model. Thus, the aim of this work is to evaluate such role and delineate the pathway involved in foetal rat myoblasts (L6) induced to differentiate by insulin—a standard and feasible model of the myogenic process. The results obtained by biochemical and morphological approaches demonstrate that (i) HMG‐CoAR increase is crucial for differentiation induction, (ii) p21waf, whose increase is a necessary requisite for differentiation to occur, rises downstream HMG‐CoAR activation, (iii) the main role of p38/MAPK as key regulator also for HMG‐CoAR. Pathologies characterized by muscle degeneration might benefit from therapeutic programmes committed to muscle function restoration, such as modulation and planning myoblast differentiation. Thus, the important role of HMG‐CoAR in muscular differentiation providing new molecular basis for the control of muscle development can help in the design of therapeutic treatment for diseases characterized by the weakening of muscular fibers and aging‐related disorders (sarcopenia). J. Cell. Physiol. 220: 524–530, 2009. © 2009 Wiley‐Liss, Inc.