Abnormal Skeletal Growth in Adolescent Idiopathic Scoliosis Is Associated with Abnormal Quantitative Expression of Melatonin Receptor, MT2
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AbstractThe defect of the melatonin signaling pathway has been proposed to be one of the key etiopathogenic factors in adolescent idiopathic scoliosis (AIS). A previous report showed that melatonin receptor, MT2, was undetectable in some AIS girls. The present study aimed to investigate whether the abnormal MT2 expression in AIS is quantitative or qualitative. Cultured osteoblasts were obtained from 41 AIS girls and nine normal controls. Semi-quantification of protein expression by Western blot and mRNA expression by TaqMan real-time PCR for both MT1 and MT2 were performed. Anthropometric parameters were also compared and correlated with the protein expression and mRNA expression of the receptors. The results showed significantly lower protein and mRNA expression of MT2 in AIS girls compared with that in normal controls (p = 0.02 and p = 0.019, respectively). No differences were found in the expression of MT1. When dichotomizing the AIS girls according to their MT2 expression, the group with low expression was found to have a significantly longer arm span (p = 0.036). The results of this study showed for the first time a quantitative change of MT2 in AIS that was also correlated with abnormal arm span as part of abnormal systemic skeletal growth.
All Author(s) ListYim APY, Yeung HY, Sun GQ, Lee KM, Ng TB, Lam TP, Ng BKW, Qiu Y, Moreau A, Cheng JCY
Journal nameInternational Journal of Molecular Sciences
Detailed descriptionTo ORKTS: doi: 10.3390/ijms14036345

Clarified by Isabel Chan, Yong Qiu is a non-CU staff, though the affiliation is stated as joint lab with our Sc
Volume Number14
Issue Number3
PublisherMDPI AG
Pages6345 - 6358
LanguagesEnglish-United Kingdom
Keywordsidiopathic scoliosis; melatonin; osteoblasts; receptors
Web of Science Subject CategoriesBiochemistry & Molecular Biology; Chemistry; Chemistry, Multidisciplinary; CHEMISTRY, MULTIDISCIPLINARY

Last updated on 2022-15-01 at 23:54