These authors contributed equally to this work.
Regulation of high mobility group box 1 and hypoxia in the migration of mesenchymal stem cells
Article first published online: 6 MAY 2014
© 2014 International Federation for Cell Biology
Cell Biology International
Volume 38, Issue 7, pages 892–897, July 2014
How to Cite
Xie, H.-L., Zhang, Y., Huang, Y.-Z., Li, S., Wu, C.-G., Jiao, X.-F., Tan, M.-Y., Huang, Y.-C. and Deng, L. (2014), Regulation of high mobility group box 1 and hypoxia in the migration of mesenchymal stem cells. Cell Biology International, 38: 892–897. doi: 10.1002/cbin.10279
- Issue published online: 2 JUN 2014
- Article first published online: 6 MAY 2014
- Accepted manuscript online: 30 MAR 2014 11:17PM EST
- Manuscript Accepted: 20 FEB 2014
- Manuscript Received: 13 JUN 2013
Mesenchymal stem cells (MSCs) have been increasingly offered for tissue regeneration with the premise that they can survive and thrive amidst the microenvironment of injured or degenerate tissues. The role of high mobility group box 1 (HMGB1) and hypoxia in the proliferation and migration of rat bone marrow MSCs (rBM-MSCs) has been investigated. First, the effect of HMGB1 on the proliferation of rBM-MSCs was determined. Second, to evaluate the regulation of hypoxia and HMGB1 in the migration of rBM-MSCs, cells in the wound healing model were exposed to four conditions: normoxia (20% O2) and complete medium, normoxia and HMGB1, hypoxia (1% O2) and complete medium, hypoxia and HMGB1. RT-PCR and Western blotting were used to measure the expression of migration-related genes and proteins. HMGB1 inhibited the proliferation of rBM-MSCs; HMGB1 alone or together with hypoxia and promoted the migration of MSCs and upregulated the expression of HIF-1α and SDF-1. These results demonstrated that HMGB1 arrested the proliferation of rBM-MSCs, but enhanced the migration of rBM-MSCs which could be further improved by hypoxia. This study strengthens current understanding of the interaction between MSCs and the microenvironment of damaged tissues.