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Estradiol via estrogen receptor beta inhibits chondrogenesis of mouse vertebral growth plate in vitro

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Abstract

Purpose

Abnormal growth of vertebral growth plate (VGP) was considered as one of the etiologic factors in adolescent idiopathic scoliosis (AIS). Previous studies described that estrogen played an important role in the pathogenesis of AIS. The present study was aimed to investigate the effect of estrogen/estrogen receptor axis on mouse VGP chondrocytes in vitro.

Methods

Chondrocytes were isolated from mouse VGP and treated with or without 17β-estradiol (E2). Cell proliferation was measured by the cell growth rate assay. Gene expression of collagen type II and aggrecan were evaluated by real-time PCR. Expression of the proliferating cell nuclear antigen (PCNA), Sox9, and Smad4 were detected by Western blotting.

Results

Estradiol inhibited the proliferation of VGP chondrocytes and the gene expression of collagen type II and aggrecan and downregulated the protein expression of PCNA, Sox9, and Smad4. In addition, the inhibitory effect of estradiol was reversed by ERβ small interfering RNA (siRNA) or PHTPP, an ERβ antagonist.

Conclusions

Estradiol via estrogen/estrogen receptor β axis inhibits the proliferation and differentiation of VGP chondrocytes, which might give some new insight into the regulatory mechanism of bone development.

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Acknowledgments

This publication was funded in part by the National Natural Science Foundation of China (81271940, 81472145) and Key Project of Natural Science Foundation of Hunan Province (12JJ2043).

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Correspondence to Hong-Qi Zhang.

Ethics declarations

The study was approved by the Ethics Committee of Xiangya Hospital of Central South University.

Conflict of interest

The authors declare that they have no conflict of interest.

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Zeng, K., Zhang, HQ., Chen, Y. et al. Estradiol via estrogen receptor beta inhibits chondrogenesis of mouse vertebral growth plate in vitro. Childs Nerv Syst 32, 461–465 (2016). https://doi.org/10.1007/s00381-015-2973-2

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  • DOI: https://doi.org/10.1007/s00381-015-2973-2

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