Concomitant activation of the PI3K/Akt and ERK1/2 signalling is involved in cyclic compressive force-induced IL-6 secretion in MLO-Y4 cells

Cell Biol Int. 2014 May;38(5):591-8. doi: 10.1002/cbin.10235. Epub 2014 Jan 10.

Abstract

IL-6 has a dual role in bone remodelling. The ERK1/2 pathway partially upregulated IL-6 secretion in osteocyte-like MLO-Y4 cells exposed to CCF. We have now investigated the possible role of phosphatidylinositol 3-kinase (PI3K)/Akt signalling pathway in the CCF-induced IL-6 expression. MLO-Y4 cells were treated with CCF 2,000 µstrain, 2 Hz, or 10, 30 min, 1, 3 and 6 h. IL-6 expression, Akt and ERK1/2 and PI3K/Akt phosphorylation were determined by RT-PCR, ELISA and Western blotting. Inhibition of PI3K/Akt with LY294002 or ERK1/2 with PD98059 significantly attenuated IL-6 upregulation, and IL-6 expression was abolished by inhibiting both pathways. Inhibition of one pathway downregulated the other's phosphorylation level. In conclusion, concomitant activation of PI3K/Akt and ERK1/2 pathways mediated IL-6 expression in MLO-Y4 cells under CCF.

Keywords: ERK1/2; PI3K/Akt; compressive force; interleukin-6; osteocyte.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Compressive Strength / physiology*
  • Enzyme Activation / physiology
  • Interleukin-6 / metabolism*
  • MAP Kinase Signaling System / physiology*
  • Osteocytes / metabolism*
  • Phosphatidylinositol 3-Kinase / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Stress, Mechanical

Substances

  • Interleukin-6
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt