Cyclic tensile force modifies calvarial osteoblast function via the interplay between ERK1/2 and STAT3

作者全名："Xiao, Xiaoyue; Zou, Shujuan; Chen, Jianwei"

作者地址："[Xiao, Xiaoyue; Zou, Shujuan; Chen, Jianwei] Sichuan Univ, State Key Lab Oral Dis, Dept Orthodont, West China Hosp Stomatol, Chengdu, Peoples R China; [Xiao, Xiaoyue; Zou, Shujuan; Chen, Jianwei] Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Dept Orthodont, Chengdu, Peoples R China; [Xiao, Xiaoyue] Chongqing Med Univ, Chongqing Key Lab Oral Dis & Biomed Sci, Stomatol Hosp, Chongqing, Peoples R China; [Xiao, Xiaoyue] Chongqing Med Univ, Chongqing Municipal Key Lab Oral Biomed Engn Highe, Stomatol Hosp, Chongqing, Peoples R China"

通信作者："Chen, JW (通讯作者)，Sichuan Univ, State Key Lab Oral Dis, Dept Orthodont, West China Hosp Stomatol, Chengdu, Peoples R China.; Chen, JW (通讯作者)，Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, Dept Orthodont, Chengdu, Peoples R China."

来源：BMC MOLECULAR AND CELL BIOLOGY

ESI学科分类：MOLECULAR BIOLOGY & GENETICS

WOS号：WOS:000945611000001

JCR分区：Q4

影响因子：2.4

年份：2023

卷号：24

期号：1

开始页：　

结束页：　

文献类型：Article

关键词：Osteoblasts; Cyclic tensile stress; Osteogenesis; ERK1; 2; STAT3

摘要："BackgroundMechanical therapies, such as distraction osteogenesis, are widely used in dental clinics. During this process, the mechanisms by which tensile force triggers bone formation remain of interest. Herein, we investigated the influence of cyclic tensile stress on osteoblasts and identified the involvement of ERK1/2 and STAT3.Materials and methodsRat clavarial osteoblasts were subjected to tensile loading (10% elongation, 0.5 Hz) for different time periods. RNA and protein levels of osteogenic markers were determined using qPCR and western blot after inhibition of ERK1/2 and STAT3. ALP activity and ARS staining revealed osteoblast mineralization capacity. The interaction between ERK1/2 and STAT3 was investigated by immunofluorescence, western blot, and Co-IP.ResultsThe results showed that tensile loading significantly promoted osteogenesis-related genes, proteins and mineralized nodules. In loading-induced osteoblasts, inhibition of ERK1/2 or STAT3 decreased osteogenesis-related biomarkers significantly. Moreover, ERK1/2 inhibition suppressed STAT3 phosphorylation, and STAT3 inhibition disrupted the nuclear translocation of pERK1/2 induced by tensile loading. In the non-loading environment, inhibition of ERK1/2 hindered osteoblast differentiation and mineralization, while STAT3 phosphorylation was elevated after ERK1/2 inhibition. STAT3 inhibition also increased ERK1/2 phosphorylation, but did not significantly affect osteogenesis-related factors.ConclusionTaken together, these data suggested that ERK1/2 and STAT3 interacted in osteoblasts. ERK1/2-STAT3 were sequentially activated by tensile force loading, and both affected osteogenesis during the process."

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