Su Liping, Qiao Qiao, Li Ruifeng, Wu Huiguang
School of Basic Medical Science, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010010, P.R. China.
Obstetrics and Gynecology Department, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia 010010, P.R. China.
Exp Ther Med. 2018 May;15(5):4185-4190. doi: 10.3892/etm.2018.5948. Epub 2018 Mar 12.
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.
受到刺激时，间充质干细胞（MSCs）可分化为成软骨细胞、脂肪细胞或成骨细胞。瘦素是一种由脂肪细胞分泌的激素，可调节食物摄入和葡萄糖稳态。本研究的目的是确定丝裂原活化蛋白激酶在瘦素诱导的兔骨髓间充质干细胞（rBMSCs）生长中的潜在作用。使用不同浓度的瘦素培养rBMSCs，观察细胞活力以及细胞外信号调节激酶1/2（ERK1/2）、c-Jun氨基末端激酶和p38磷酸化状态的变化。结果显示，瘦素处理的rBMSCs的生长主要受到磷酸化ERK1/2的抑制，这是由瘦素受体介导的。总之，本研究结果表明，瘦素主要通过ERK1/2信号通路抑制rBMSCs的生长。
