期刊
INTERNATIONAL JOURNAL OF PEPTIDE RESEARCH AND THERAPEUTICS
卷 20, 期 4, 页码 421-425出版社
SPRINGER
DOI: 10.1007/s10989-014-9404-1
关键词
Proliferation; Apelin; Bone marrow-derived mesenchymal stem cells
资金
- National Natural Science Foundation of China [81270420, 81070634]
- Heng Yang Joint Funds of Hunan Provincial Natural Science Foundation of China [12JJ8013]
- Hunan Provincial Natural Science Foundation of China [14JJ3102]
The migration and proliferation of bone marrow-derived mesenchymal stem cells (BMSC) is critical to treatment of ischemic injury. Apelin is a recently discovered vasoactive peptide, which has been demonstrated to be the endogenous ligand for the previously orphaned G protein-coupled receptor, angiotensin-like 1 receptor. Apelin has mitogenic effects on a wide variety of cell types. However, the effects of apelin on BMSC proliferation have not been evaluated. We hypothesize that the peptide apelin-13 may enhance BMSC proliferation. Rat BMSC obtain from the bone marrow of 3- to 4-month-old SD rats. There are novel data suggesting that apelin-13 significantly simulates BMSC proliferation and promotes the expression of p-AKT, p-GSK3 beta and cyclin D1 in a concentration-dependent manner. Apelin-13-induced the increases of p-AKT, p-GSK3 beta and cyclin D1 could be abolished by LY294002 (AKT inhibitor) which prevents apelin-13-induced BMSC proliferation. However, LiCl (GSK inhibitor) up-regulates the expression of p-GSK3 beta and cyclin D1, promotes BMSC proliferation, which enhances the proliferation effect of apelin-13 obviously. In conclusion, the AKT/GSK3 beta/cyclin D1 signaling pathway is involved in apelin-13-induced BMSC proliferation.
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