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Skeletal muscle myogenesis is regulated by G protein-coupled receptor kinase 2

Journal of Molecular Cell Biology 2014年第4期8卷 299-311页

作者： Lucia Garcia-Guerra Rocio Vila-Bedmar Marta carrasco-Rando Marta Cruces-Sande Mercedes Martin Ana Ruiz-Gomez Mar Ruiz-Gomez Margarita Lorenzo Sonia Fernandez-Veledo Federico Mayor Jr. cristina Murga Iria Nieto-Vazquez Department of Biochemistry and Molecular Biology II School of Pharmacy Complutense University 28040 Madrid Spain CIBER de Diabetes y Enfermedades Metab61icas Asociadas (CIBERDEM) 08017 Barcelona Spain Instituto de Investigaciones Biomedicas Alberto Sols (CSIC-UAM) 28029 Madrid Spain CIBER de enfermedades neurodegenerativas (CIBERNED) 28049 Madrid Spain Departament of Molecular Biology and Centro de Biologia Molecular Severo Ochoa (CSIC-UAM) 28049 Madrid Spain Instituto de Investigacion Sanitaria la Princesa 28006 Madrid Spain Centro de Biologia Molecular Severo Ochoa (UAM-CSIC) 28049 Madrid Spain Hospital Universitari de Tarragona Joan XXIII. IISPV. Universitat Rovira i Virgili 43007 Tarragona Spain

G protein-coupled receptor kinase 2 （GRK2） is an important serine/threonine-kinase regulating different membrane receptors and intraceUular proteins. Attenuation of Drosophila Gprk2 in embryos or adult flies induced a defective differentiation of somatic muscles, loss of fibers, and a flightless phenotype. In vertebrates, GRK2 hemizygous mice contained less but more hypertrophied skeletal muscle fibers than wild-type littermates. In C2C12 myoblasts, overexpression of a GRK2 kinase-deficient mutant （K220R） caused precocious differentiation of ceUs into immature myotubes, which were wider in size and contained more fused nuclei, while GRK2 overexpression blunted differentiation. Moreover, p38MAPK and Akt pathways were activated at an earlier stage and to a greater extent in K220R-expressing cells or upon kinase downregulation, while the activation of both kinases was impaired in GRK2-overexpressing cells. The impaired differentiation and fewer fusion events promoted by enhanced GRK2 levels were recapitulated by a p38MAPK mutant, which was able to mimic the inhibitory phosphorylation of p38MAPK by GRK2, whereas the blunted differentiation observed in GRK2-expressing clones was rescued in the presence of a constitutively active upstream stimulator of the p38MAPK pathway. These results suggest that balanced GRK2 function is necessary for a timely and complete myogenic process.

关键词： GRK2 p38MAPK Akt skeletal muscle myogenesis

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