Next Article in Journal
Immune Checkpoint Inhibitors: A New Opportunity in the Treatment of Ovarian Cancer?
Next Article in Special Issue
Development of a Patient-Derived Xenograft (PDX) of Breast Cancer Bone Metastasis in a Zebrafish Model
Previous Article in Journal
Structural Analysis of Hand Drawn Bumblebee Bombus terrestris Silk
Previous Article in Special Issue
Bone Metastasis from Renal Cell Carcinoma
Article Menu
Issue 7 (July) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2016, 17(7), 1160;

Leptin Receptor Metabolism Disorder in Primary Chondrocytes from Adolescent Idiopathic Scoliosis Girls

Department of Spine Surgery, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha 410008, China
Author to whom correspondence should be addressed.
Academic Editor: Maria Alfonsina Desiderio
Received: 26 May 2016 / Revised: 27 June 2016 / Accepted: 11 July 2016 / Published: 20 July 2016
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Bone Metastasis)
Full-Text   |   PDF [9951 KB, uploaded 20 July 2016]   |  


To investigate the underlying mechanisms of low metabolic activity of primary chondrocytes obtained from girls with adolescent idiopathic scoliosis (AIS); AIS is a spine-deforming disease that often occurs in girls. AIS is associated with a lower bone mass than that of healthy individuals and osteopenia. Leptin was shown to play an important role in bone growth. It can also regulate the function of chondrocytes. Changes in leptin and Ob-R levels in AIS patients have been reported in several studies. The underlying mechanisms between the dysfunction of peripheral leptin signaling and abnormal chondrocytes remain unclear; The following parameters were evaluated in AIS patients and the control groups: total serum leptin levels; Ob-R expression in the plasma membrane of primary chondrocytes; JAK2 and STAT3 phosphorylation status. Then, we inhibited the lysosome and proteasome and knocked down clathrin heavy chain (CHC) expression in primary chondrocytes isolated from girls with AIS and evaluated Ob-R expression. We investigated the effects of leptin combined with a lysosome inhibitor or CHC knockdown in primary chondrocytes obtained from AIS patients; Compared with the controls, AIS patients showed similar total serum leptin levels, reduced JAK2 and STAT3 phosphorylation, and decreased cartilage matrix synthesis in the facet joint. Lower metabolic activity and lower membrane expression of Ob-R were observed in primary chondrocytes from the AIS group than in the controls. Lysosome inhibition increased the total Ob-R content but had no effect on the membrane expression of Ob-R or leptin’s effects on AIS primary chondrocytes. CHC knockdown upregulated the membrane Ob-R levels and enhanced leptin’s effects on AIS primary chondrocytes; The underlying mechanism of chondrocytes that are hyposensitive to leptin in some girls with AIS is low plasma membrane Ob-R expression that results from an imbalance between the rate of receptor endocytosis and the insertion of newly synthesized receptors into the membrane. View Full-Text
Keywords: leptin; Ob-R; adolescent idiopathic scoliosis; pathogenesis leptin; Ob-R; adolescent idiopathic scoliosis; pathogenesis

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Wang, Y.-J.; Yu, H.-G.; Zhou, Z.-H.; Guo, Q.; Wang, L.-J.; Zhang, H.-Q. Leptin Receptor Metabolism Disorder in Primary Chondrocytes from Adolescent Idiopathic Scoliosis Girls. Int. J. Mol. Sci. 2016, 17, 1160.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top