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Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis

Abnormalities in the melatonin signaling pathway and the involvement of melatonin receptor MT2 have been reported in patients with adolescent idiopathic scoliosis (AIS). Whether these abnormalities were involved in the systemic abnormal skeletal growth in AIS during the peripubertal period remain un...

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Autores principales: Wang, William Wei-Jun, Man, Gene Chi-Wai, Wong, Jack Ho, Ng, Tzi-Bun, Lee, Kwong-Man, Ng, Bobby Kin-Wah, Yeung, Hiu-Yan, Qiu, Yong, Cheng, Jack Chun-Yiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200781/
https://www.ncbi.nlm.nih.gov/pubmed/25257530
http://dx.doi.org/10.3390/ijms150917100
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author Wang, William Wei-Jun
Man, Gene Chi-Wai
Wong, Jack Ho
Ng, Tzi-Bun
Lee, Kwong-Man
Ng, Bobby Kin-Wah
Yeung, Hiu-Yan
Qiu, Yong
Cheng, Jack Chun-Yiu
author_facet Wang, William Wei-Jun
Man, Gene Chi-Wai
Wong, Jack Ho
Ng, Tzi-Bun
Lee, Kwong-Man
Ng, Bobby Kin-Wah
Yeung, Hiu-Yan
Qiu, Yong
Cheng, Jack Chun-Yiu
author_sort Wang, William Wei-Jun
collection PubMed
description Abnormalities in the melatonin signaling pathway and the involvement of melatonin receptor MT2 have been reported in patients with adolescent idiopathic scoliosis (AIS). Whether these abnormalities were involved in the systemic abnormal skeletal growth in AIS during the peripubertal period remain unknown. In this cross-sectional case-control study, growth plate chondrocytes (GPCs) were cultured from twenty AIS and ten normal control subjects. Although the MT2 receptor was identified in GPCs from both AIS and controls, its mRNA expression was significantly lower in AIS patients than the controls. GPCs were cultured in the presence of either the vehicle or various concentrations of melatonin, with or without the selective MT2 melatonin receptor antagonist 4-P-PDOT (10 µM). Then the cell viability and the mRNA expression of collagen type X (COLX) and alkaline phosphatase (ALP) were assessed by MTT and qPCR, respectively. In the control GPCs, melatonin at the concentrations of 1, 100 nM and 10 µM significantly reduced the population of viable cells, and the mRNA level of COLX and ALP compared to the vehicle. Similar changes were not observed in the presence of 4-P-PDOT. Further, neither proliferation nor differentiation of GPCs from AIS patients was affected by the melatonin treatment. These findings support the presence of a functional abnormality of the melatonin signaling pathway in AIS GPCs, which might be associated with the abnormal endochondral ossification in AIS patients.
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spelling pubmed-42007812014-10-17 Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis Wang, William Wei-Jun Man, Gene Chi-Wai Wong, Jack Ho Ng, Tzi-Bun Lee, Kwong-Man Ng, Bobby Kin-Wah Yeung, Hiu-Yan Qiu, Yong Cheng, Jack Chun-Yiu Int J Mol Sci Article Abnormalities in the melatonin signaling pathway and the involvement of melatonin receptor MT2 have been reported in patients with adolescent idiopathic scoliosis (AIS). Whether these abnormalities were involved in the systemic abnormal skeletal growth in AIS during the peripubertal period remain unknown. In this cross-sectional case-control study, growth plate chondrocytes (GPCs) were cultured from twenty AIS and ten normal control subjects. Although the MT2 receptor was identified in GPCs from both AIS and controls, its mRNA expression was significantly lower in AIS patients than the controls. GPCs were cultured in the presence of either the vehicle or various concentrations of melatonin, with or without the selective MT2 melatonin receptor antagonist 4-P-PDOT (10 µM). Then the cell viability and the mRNA expression of collagen type X (COLX) and alkaline phosphatase (ALP) were assessed by MTT and qPCR, respectively. In the control GPCs, melatonin at the concentrations of 1, 100 nM and 10 µM significantly reduced the population of viable cells, and the mRNA level of COLX and ALP compared to the vehicle. Similar changes were not observed in the presence of 4-P-PDOT. Further, neither proliferation nor differentiation of GPCs from AIS patients was affected by the melatonin treatment. These findings support the presence of a functional abnormality of the melatonin signaling pathway in AIS GPCs, which might be associated with the abnormal endochondral ossification in AIS patients. MDPI 2014-09-25 /pmc/articles/PMC4200781/ /pubmed/25257530 http://dx.doi.org/10.3390/ijms150917100 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Wang, William Wei-Jun
Man, Gene Chi-Wai
Wong, Jack Ho
Ng, Tzi-Bun
Lee, Kwong-Man
Ng, Bobby Kin-Wah
Yeung, Hiu-Yan
Qiu, Yong
Cheng, Jack Chun-Yiu
Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title_full Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title_fullStr Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title_full_unstemmed Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title_short Abnormal Response of the Proliferation and Differentiation of Growth Plate Chondrocytes to Melatonin in Adolescent Idiopathic Scoliosis
title_sort abnormal response of the proliferation and differentiation of growth plate chondrocytes to melatonin in adolescent idiopathic scoliosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4200781/
https://www.ncbi.nlm.nih.gov/pubmed/25257530
http://dx.doi.org/10.3390/ijms150917100
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