Low frequency pulsed electromagnetic field promotes C2C12 myoblasts proliferation via activation of MAPK/ERK pathway

Biochem Biophys Res Commun. 2016 Oct 7;479(1):97-102. doi: 10.1016/j.bbrc.2016.09.044. Epub 2016 Sep 11.

Abstract

Low frequency pulsed electromagnetic field (PEMF) has been shown to affect the activity of various cell types and promote them proliferation. However, its effect on skeletal muscle cells remains to be determined. In our study, we confirmed that PEMF (100 Hz, 1 mT) could promote C2C12 myoblasts proliferation by using Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assays, yet hardly any distinction was found in the rate of cell apoptosis between PEMF and control groups by flow cytometry (Annexin V-FITC/PI double staining method). To further study the mechanism of action of PEMF, Western blot was utilized to detect the mitogen-activated protein kinase (MAPK) signaling pathways. After exposing C2C12 myoblasts to PEMF, we found the phosphorylation level of extracellular signal-regulated kinase (ERK) was significantly increased, while p38 MAPK and c-Jun N-terminal kinase (JNK) pathways were not affected. Pretreating the cells with the ERK kinase1/2 (MEK1/2) inhibitor U0126 obviously inhibited the proliferation of C2C12 cells. Taken together, our research for the first time demonstrated that PEMF promoted C2C12 myoblasts proliferation via activating MAPK/ERK pathway.

Keywords: C2C12 myoblasts; MAPK/ERK pathway; Proliferation; Pulsed electromagnetic field.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Blotting, Western
  • Butadienes / pharmacology
  • Cell Line
  • Cell Proliferation / drug effects
  • Cell Proliferation / physiology*
  • Electromagnetic Fields*
  • Enzyme Inhibitors / pharmacology
  • Flow Cytometry
  • MAP Kinase Signaling System / drug effects
  • MAP Kinase Signaling System / physiology
  • Mice
  • Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 1 / metabolism*
  • Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 3 / metabolism*
  • Myoblasts / cytology
  • Myoblasts / metabolism*
  • Nitriles / pharmacology
  • p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Butadienes
  • Enzyme Inhibitors
  • Nitriles
  • U 0126
  • Mapk1 protein, mouse
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • p38 Mitogen-Activated Protein Kinases