[TNF-α stimulates bone marrow mesenchymal stem cell VCAM-1 production by ERK signaling pathway]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2013 Dec;21(6):1568-71. doi: 10.7534/j.issn.1009-2137.2013.06.038.
[Article in Chinese]

Abstract

This study was aimed to explore the effect of TNF-α on the vascular cell adhesion molecule 1 (VCAM-1) expression of human bone marrow mesenchymal stem cells (BMMSC) and the relationship between this process and ERK signalling pathway. BMMSC were isolated by density gradient centrifugation combined with adherent culture method, and then identified by surface antigen expression and differentiation potential. Flow cytometry was used to detect expression of VCAM-1 on BMMSC exposed to TNF-α at different concentrations, and the effect of ERK inhibitor U0126 on VCAM-1 of BMMSC. ERK signaling pathway activation was analyzed by Western blot. The results showed that BMMSC positively expressed CD29, CD69, CD44, CD105, and negatively expressed CD34, CD45. BMMSC could be induced to differentiate into osteoblasts and adipocytes. Flow cytometry analysis showed that after the TNF-α stimulation, the expression of VCAM-1 on BMMSC increased in a dose-dependent manner. And this increase was inhibited by U0126. TNF-α caused activation of ERK signal pathway, and U0126 suppressed this effect induced by TNF-α. It is concluded that TNF-α can increase expression of VCAM-1 of BMMSC via ERK signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bone Marrow Cells / cytology
  • Bone Marrow Cells / drug effects
  • Bone Marrow Cells / metabolism*
  • Cells, Cultured
  • Humans
  • MAP Kinase Signaling System / drug effects*
  • Mesenchymal Stem Cells / cytology
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Vascular Cell Adhesion Molecule-1 / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • Vascular Cell Adhesion Molecule-1