Abstract
When stimulated, mesenchymal stem cells (MSCs) may differentiate into chondroblasts, adipocytes or osteoblasts. Leptin is an adipocyte-derived hormone, which regulates food intake and glucose homeostasis. The aim of the present study was to identify the potential role of mitogen-activated protein kinase in the leptin-induced growth of rabbit bone MSCs (rBMSCs). Various concentrations of leptin were used to culture rBMSCs and the viability of cells was observed as well as alterations in the phosphorylation state of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase and p38. It was revealed that the growth of leptin-treated rBMSCs was primarily inhibited by phosphorylated ERK1/2, which was mediated by the leptin receptor. In conclusion, the results of the present study demonstrated that leptin inhibits the growth of rBMSCs principally via the ERK1/2 signaling pathway.