Differentiation |
Healthy BM-MSC overexpressing leptin or treated with exogenous leptin |
Inhibited adipogenesis but promoted osteogenesis |
45,47 |
Osteoporotic rat-derived BM-MSC stimulated with leptin |
Failed to induce osteogenesis |
48,49 |
HFD obese mouse-derived BM-MSC |
High serum leptin levels inhibited osteogenesis but promoted adipogenesis |
50 |
Cell survival, proliferation, and senescence |
BM-MSC preconditioned with hypoxia |
Leptin upregulation by hypoxia conferred survival advantages to MSC by activating autophagy |
53 |
BM-MSC overexpressing leptin |
Decreased apoptosis under hypoxic and serum deprivation culture conditions; increased viability upon transplantation |
55 |
UM-MSC treated with leptin or serum from systemic lupus erythematosus (SLE) patients |
Long-term treatment with leptin or SLE serum containing high levels of leptin-induced cell senescence. |
56 |
ob/ob mice treated with leptin |
Leptin treatment increased the yield of MSC in the adipose-derived stromal vascular fraction and enhanced the expression of MCP-1 in adipose tissue and in ob/ob mouse-derived MSC |
58 |
Therapeutic effects |
BM-MSC preconditioned with hypoxia |
Hypoxia-induced endogenous leptin expression was required to enhance the cardioprotective effects of MSCs |
54 |
BM-MSC overexpressing leptin |
Enhanced the protective efficacy against myocardial infarction |
55 |