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Abnormal melatonin receptor 1B expression in osteoblasts from girls with adolescent idiopathic scoliosis

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Abstract: 

Melatonin signaling dysfunction has been associated with the etiology of adolescent idiopathic scoliosis (AIS). Genetic analysis has also associated the occurrence of AIS with the MT2 gene. Thus, we determined whether there is abnormality in the protein expression of melatonin receptors (MT) in AIS osteoblasts. In this study, we recruited 11 girls with severe AIS and eight normal subjects for intraoperative bone biopsies. MT1 and MT2 receptor protein expressions in the isolated osteoblasts were detected. Also, cell proliferation assay using different melatonin concentrations (0, 10−9, 10−5, 10−4 m) was carried out. The results showed that both MT1 and MT2 receptors are expressed in osteoblasts of the controls. While MT1 receptors were expressed in osteoblasts of all AIS subjects, osteoblasts of only 7 of 11 AIS showed expression of MT2 receptors. Melatonin stimulated control osteoblasts to proliferate. However, proliferation of AIS osteoblasts without expression of MT2 receptor, after treatment with melatonin, was minimal when compared with control and AIS osteoblasts with MT2 receptor expression. The proliferation of AIS osteoblasts with MT2 receptor was greater than those without. This is the first report demonstrating a difference between AIS and normal osteoblasts in the protein expression of MT2 receptor. The results suggest that there is a possible functional effect of MT2 receptor on osteoblast proliferation. AIS osteoblasts without expression of MT2 receptor showed the lowest percentage of viable cells after melatonin treatment. This possibly indicates the modulating role of melatonin through MT2 receptor on the proliferation of osteoblasts.
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Keywords: idiopathic scoliosis; melatonin; osteoblasts; proliferation; receptor

Document Type: Research Article

Affiliations: 1: Department of Orthopedics & Traumatology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 2: School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong 3: Lee Hysan Clinical Research Laboratory, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong

Publication date: May 1, 2011

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