Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 47, Issue 5, Pages 362-367Publisher
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gmv014
Keywords
hypoxia; apelin; mesenchymal stem cell; autophagy; proliferation
Categories
Funding
- National Natural Science Foundation of China [81470434, 81270420]
- Hunan Provincial Natural Science Foundation [14JJ3102]
- China Postdoctoral Science Foundation [2014M560647]
- Program for Science and Technology Innovative Research Team in Higher Educational Institutions of Hunan Province [2008-244]
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Bone marrow-derived mesenchymal stem cells (BMSCs) are a population of multipotent progenitors that have the capacity of proliferation and differentiation into mesenchymal lineage cells. The regulatory peptide apelin is the endogenous ligand for the G protein-coupled receptor APJ. Apelin, which can enhance BMSC proliferation, has mitogenic effects on a wide variety of cell types. We hypothesized that the increased apelin/APJ might be involved in the occurrence and development of hypoxia-induced BMSC proliferation. BMSCs from the bone marrow of 8- to 10-week-old C57BL/6J mice were cultured under either normoxia (21% oxygen) or hypoxia (1% oxygen) condition. Cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and 5-bromo-2'-deoxyuridine assay. Expressions of hypoxia-inducible factor (HIF)-1 alpha, apelin, APJ, Beclin-1, and LC3II/LC3I were detected by western blot analysis. Results suggested that hypoxia enhanced the proliferation of BMSC in a time-dependent manner. The expressions of HIF-1 alpha, apelin, APJ, Beclin-1, and LC3II/LC3I were increased in BMSCs induced by hypoxia. Small interfering RNA (siRNA)-HIF-1 alpha that inhibited the hypoxia-induced expressions of apelin, APJ, Beclin-1, and LC3II/LC3I prevented hypoxia-induced BMSC proliferation. siRNA-APJ that inhibited the hypoxia-induced expressions of Beclin-1 and LC3II/LC3I reversed hypoxia-induced BMSC proliferation. siRNA-Beclin-1 also abolished hypoxia-induced cell proliferation. These data suggested that the apelin/APJ/autophagy signaling pathway might be involved in hypoxia-induced BMSC proliferation.
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