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Acta Physiologica 2006; Volume 186, Supplement 650
Joint Meeting of The German Society of Physiology and The Federation of European Physiological Societies 2006
3/26/2006-3/29/2006
Ludwig-Maximilians-University, Munich
THE P38 BUT NOT THE ERK MAPK ACTIVATES THE FAST MHCIID/X PROMOTER IN C2C12 MYOTUBES
Abstract number: OM03-14
Meissner1 JD, Chang2 KC, Gros1 G, Scheibe1 RJ
1Department of Physiology, Hannover Medical School, Hannover, Germany
2Institute of Comparative Medicine, University of Glasgow Veterinary School, Glasgow, U.K.
The role of mitogen-activated protein kinases (MAPKs) for the regulation of fast myosin heavy chain (MHC) IId/x promoter basal activity and Ca2+-ionophore-induced downregulation during fast-to-slow transformation was investigated in C2C12 myotubes. C2C12 cells were transiently transfected with a -2.8 kb MHCIId/x promoter luciferase construct. Maintenance of the high level of basal promoter activity required active p38 MAPK. Basal activity was further induced by the transcription factor myocyte enhancer factor-2 (MEF-2) isoforms C and D, which bind to a proximal MEF-2 consensus site in the promoter. MEF-2C was found to partly mediate the effect of p38 MAPK. Treatment with Ca2+-ionophore reduced p38 MAPK activation and MHCIId/x promoter activity, while enforced activation of p38 by constitutively active MAPK kinase 6 (MKK6EE) diminished the effect of Ca2+-ionophore. In contrast, the ERK MAPK pathway was not involved in MHCIId/x promoter regulation. The data demonstrate the importance of p38 MAPK for activation of the fast MHCIId/x gene. The work was supported by DFG grant GR489/13.
To cite this abstract, please use the following information:
Acta Physiologica 2006; Volume 186, Supplement 650 :OM03-14