Leptin Antagonizes Peroxisome Proliferator-Activated Receptor-γ Signaling in Growth Plate Chondrocytes.
Leptin Antagonizes Peroxisome Proliferator-Activated Receptor-γ Signaling in Growth Plate Chondrocytes.
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瘦素拮抗生长板软骨细胞中的过氧化物酶体增殖物激活受体-γ信号传导。
DOI：
10.1155/2012/756198
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发表时间：
2012
期刊：
影响因子：
2.9
通讯作者：
Ballock,RTracy
中科院分区：
文献类型：
--
作者：
Wang,Lai;Shao,YvonneY;Ballock,RTracy
Leptin is an obesity‐associated cytokine‐like hormone encoded by theobgene. Recent studies reveal that leptin promotes proliferation and differentiation of chondrocytes, suggesting a peripheral role of leptin in regulating growth plate function. Peroxisome proliferator‐activated receptor‐γ(PPARγ) is a transcriptional regulator of adipogenesis. Locally, PPARγnegatively regulates chondrogenic differentiation and terminal differentiation in the growth plate. The aim of this study was to test the hypothesis that leptin may suppress the inhibitory effects of PPARγon growth plate chondrocytes. Chondrocytes were collected from distal femoral growth plates of newborn rats and were cultured in monolayer or cell pellets in the presence or absence of leptin and the PPARγagonist ciglitazone. The results show that leptin attenuates the suppressive effects of PPARγon chondrogenic differentiation and T3‐mediated chondrocyte hypertrophy. Leptin treatment also leads to a mild downregulation of PPAR mRNA expression and a significant MAPK/ERK‐dependent PPARγphosphorylation at serine 112/82. Blocking MAPK/ERK function with PD98059 confirmed that leptin antagonizes PPARγfunction in growth plate chondrocytes through the MAPK/ERK signaling pathway. Furthermore, leptin signaling in growth plate cells is also negatively modulated by activation of PPARγ, implying that these two signaling pathways are mutually regulated in growth plate chondrocytes.
