Leptin Induces Terminal Differentiation of Rat Annulus Fibrosus Cells via Activation of MAPK Signaling

被引：18

作者：

Ding, Wei ^{[1
]}

Zhao, Changqing ^{[1
]}

Cao, Lei ^{[2
]}

Zhang, Kai ^{[1
]}

Sun, Wei ^{[1
]}

Xie, Youzhuanu ^{[1
]}

Li, Hua ^{[1
]}

Zhao, Jie ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Sch Med, Shanghai Peoples Hosp 9, Dept Orthopaed,Shanghai Key Lab Orthopaed Implant, Shanghai 200011, Peoples R China

[2] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 1, Dept Orthopaed, Shanghai 200011, Peoples R China

来源：

ANATOMICAL RECORD-ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY | 2013年 / 296卷 / 12期

基金：

中国国家自然科学基金;

关键词：

leptin; MAPK; terminal differentiation; annulus fibrosus cells; HUMAN INTERVERTEBRAL DISC; NUCLEUS PULPOSUS CELLS; CHONDROCYTE DIFFERENTIATION; MATRIX METALLOPROTEINASES; BASIC SCIENCE; UP-REGULATION; EXPRESSION; DEGRADATION; INHIBITION; TISSUE;

D O I：

10.1002/ar.22806

中图分类号：

R602 [外科病理学、解剖学]; R32 [人体形态学];

学科分类号：

100123 [人体微生态学]; 100210 [外科学];

摘要：

Both leptin and its receptor are expressed in rat annulus fibrosus (AF) cells. However, little is known about their role and mechanism during disc degeneration. The mitogen activating protein kinase (MAPK) pathway which mediates leptin-induced terminal differentiation of rat AF cells was analyzed using PCR, Western-blot and immunocytochemistry. It was found that leptin-induced AF cells terminal differentiation, which may be attributed to upregulated p38 and ERK1/2 phosphorylation, however, JNK phosphorylation was not observed. Specific inhibitors of p38 or ERK1/2, but not JNK, could inhibit the stimulative activity of leptin on collagen X and MMP-13 protein levels. This study, for the first time, shows that the MAPK pathway, especially p38 and ERK1/2 signaling, plays a distinct role in leptin-induced AF cells terminal differentiation. Anat Rec, 296:1806-1812, 2013. (c) 2013 Wiley Periodicals, Inc.

引用

页码：1806 / 1812

页数：7

共 42 条

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Leptin regulates chondrogenic differentiation in ATDC5 cell-line through JAK/STAT and MAPK pathways [J].