Creatine enhances differentiation of myogenic C2C12 cells by activating both p38 and Akt/PKB pathways

Am J Physiol Cell Physiol. 2007 Oct;293(4):C1263-71. doi: 10.1152/ajpcell.00162.2007. Epub 2007 Jul 25.

Abstract

In myogenic C(2)C(12) cells, 5 mM creatine increased the incorporation of labeled [(35)S]methionine into sarcoplasmic (+20%, P < 0.05) and myofibrillar proteins (+50%, P < 0.01). Creatine also promoted the fusion of myoblasts assessed by an increased number of nuclei incorporated within myotubes (+40%, P < 0.001). Expression of myosin heavy chain type II (+1,300%, P < 0.001), troponin T (+65%, P < 0.01), and titin (+40%, P < 0.05) was enhanced by creatine. Mannitol, taurine, and beta-alanine did not mimic the effect of creatine, ruling out an osmolarity-dependent mechanism. The addition of rapamycin, the inhibitor of mammalian target of rapamycin/70-kDa ribosomal S6 protein kinase (mTOR/p70(s6k)) pathway, and SB 202190, the inhibitor of p38, completely blocked differentiation in control cells, and creatine did not reverse this inhibition, suggesting that the mTOR/p70(s6k) and p38 pathways could be potentially involved in the effect induced by creatine on differentiation. Creatine upregulated phosphorylation of protein kinase B (Akt/PKB; +60%, P < 0.001), glycogen synthase kinase-3 (+70%, P < 0.001), and p70(s6k) (+50%, P < 0.001). Creatine also affected the phosphorylation state of p38 (-50% at 24 h and +70% at 96 h, P < 0.05) as well as the nuclear content of its downstream targets myocyte enhancer factor-2 (-55% at 48 h and +170% at 96 h, P < 0.05) and MyoD (+60%, P < 0.01). In conclusion, this study points out the involvement of the p38 and the Akt/PKB-p70(s6k) pathways in the enhanced differentiation induced by creatine in C(2)C(12) cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Differentiation / drug effects*
  • Cell Differentiation / physiology
  • Cell Line
  • Connectin
  • Creatine / metabolism
  • Creatine / pharmacology*
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glycogen Synthase Kinase 3 / metabolism
  • Imidazoles / pharmacology
  • MEF2 Transcription Factors
  • Mice
  • Models, Biological
  • Muscle Development / drug effects
  • Muscle Development / physiology
  • Muscle Proteins / metabolism
  • MyoD Protein / metabolism
  • Myoblasts / cytology
  • Myoblasts / drug effects*
  • Myoblasts / metabolism
  • Myogenic Regulatory Factors / metabolism
  • Myosin Heavy Chains / metabolism
  • Phosphocreatine / metabolism
  • Phosphorylation / drug effects
  • Podophyllotoxin / analogs & derivatives
  • Podophyllotoxin / pharmacology
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Pyridines / pharmacology
  • Receptor, IGF Type 1 / antagonists & inhibitors
  • Ribosomal Protein S6 Kinases, 70-kDa / metabolism
  • Signal Transduction
  • Troponin T / metabolism
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Connectin
  • Imidazoles
  • MEF2 Transcription Factors
  • Muscle Proteins
  • MyoD Protein
  • MyoD1 myogenic differentiation protein
  • Myogenic Regulatory Factors
  • Protein Kinase Inhibitors
  • Pyridines
  • Troponin T
  • Phosphocreatine
  • picropodophyllin
  • Protein Kinases
  • Receptor, IGF Type 1
  • Proto-Oncogene Proteins c-akt
  • Ribosomal Protein S6 Kinases, 70-kDa
  • Extracellular Signal-Regulated MAP Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Glycogen Synthase Kinase 3
  • Myosin Heavy Chains
  • Podophyllotoxin
  • Creatine
  • 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole