过表达Wnt7b可拮抗地塞米松对ST2细胞成骨的抑制作用。

IF 2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Endokrynologia Polska Pub Date : 2023-01-01 DOI:10.5603/EP.a2022.0035

Yuan Gu, Yongquan Gao, Zhanghuan Yang, Jiangdong Ni, Guangxu He

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引用次数: 0

摘要

糖皮质激素诱导的骨质疏松症与成骨前细胞的分化和功能密切相关。本研究的前提是Wnt7b可以通过Wnt信号通路促进骨形成，因为它可以刺激成骨前细胞分化并增加其活性。然而，外源性糖皮质激素导致的成骨细胞分化和功能受到抑制，Wnt7b是否能恢复尚不清楚。材料与方法:本研究利用过表达Wnt7b的ST2细胞，探讨Wnt7b是否能挽救被抑制的成骨细胞的分化和功能，为研究治疗糖皮质激素所致骨质疏松症的新药提供有力证据。结果/结论:我们发现Wnt7b可以恢复地塞米松引起的成骨细胞分化和功能抑制。

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Overexpression of Wnt7b antagonizes the inhibitory effect of dexamethasone on osteoblastogenesis of ST2 cells.

Introduction: It is well established that glucocorticoid-induced osteoporosis is highly associated with preosteoblast differentiation and function. This study is based on the premise that Wnt7b can promote bone formation through Wnt signalling pathway because it can stimulate preosteoblast differentiation and increase its activity. However, it is unknown whether Wnt7b can rescue the inhibited osteoblast differentiation and function caused by exogenous glucocorticoid.

Material and methods: In this study we used Wnt7b overexpression ST2 cells to explore whether Wnt7bcan rescue the inhibited osteoblast differentiation and function, which can provide strong proof to investigate a new drug for curing the glucocorticoid induced osteoporosis.

Results/conclusion: We found that Wnt7b can rescue the suppressed osteoblast differentiation and function without cell viability caused by dexamethasone.

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来源期刊

Endokrynologia Polska ENDOCRINOLOGY & METABOLISM-

CiteScore

2.60

自引率

9.50%

发文量

129

审稿时长

6-12 weeks

期刊介绍： "Endokrynologia Polska" publishes papers in English on all aspects of clinical and experimental endocrinology. The following types of papers may be submitted for publication: original articles, reviews, case reports, postgraduate education, letters to the Editor (Readers’ Forum) and announcements of scientific meetings, conferences and congresses.