ATP6V1H facilitates osteogenic differentiation in MC3T3-E1 cells via Akt/GSK3β signaling pathway.

IF 1.6 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Organogenesis Pub Date : 2019-01-01 Epub Date: 2019-07-04 DOI:10.1080/15476278.2019.1633869

Fusong Jiang, Haojie Shan, Chenhao Pan, Zubin Zhou, Keze Cui, Yuanliang Chen, Haibo Zhong, Zhibin Lin, Nan Wang, Liang Yan, Xiaowei Yu

{"title":"ATP6V1H facilitates osteogenic differentiation in MC3T3-E1 cells via Akt/GSK3β signaling pathway.","authors":"Fusong Jiang, Haojie Shan, Chenhao Pan, Zubin Zhou, Keze Cui, Yuanliang Chen, Haibo Zhong, Zhibin Lin, Nan Wang, Liang Yan, Xiaowei Yu","doi":"10.1080/15476278.2019.1633869","DOIUrl":null,"url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of all diabetic patients, and osteoporosis is one of the complications during T2DM process. ATP6V1H (V-type proton ATPase subunit H) displays crucial roles in inhibiting bone loss, but its role in osteogenic differentiation remains unknown. Therefore in this study, we aimed to explore the biological role of ATP6V1H in osteogenic differentiation. OM (osteogenic medium) and HG (high glucose and free fatty acids) were used to induce the MC3T3-E1 cells into osteogenic differentiation in a T2DM simulating environment. CCK8 assay was used to detect cell viability. Alizarin Red staining was used to detect the influence of ATP6V1H on osteogenic differentiation. ATP6V1H expression increased in OM-MC3T3-E1 cells, while decreased in OM+HG-MC3T3-E1 cells. ATP6V1H promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. Overexpression of ATP6V1H inhibited Akt/GSK3β signaling pathway, while knockdown of ATP6V1H promoted Akt/GSK3β signaling pathway. ATP6V1H overexpression promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. The role of ATP6V1H in osteogenic differentiation in a T2DM simulating environment involved in Akt/GSK3β signaling pathway. These data demonstrated that ATP6V1H could serve as a potential target for osteogenic differentiation in a T2DM simulating environment.</p>","PeriodicalId":19596,"journal":{"name":"Organogenesis","volume":"15 2","pages":"43-54"},"PeriodicalIF":1.6000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15476278.2019.1633869","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Organogenesis","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1080/15476278.2019.1633869","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2019/7/4 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 6

Abstract

Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of all diabetic patients, and osteoporosis is one of the complications during T2DM process. ATP6V1H (V-type proton ATPase subunit H) displays crucial roles in inhibiting bone loss, but its role in osteogenic differentiation remains unknown. Therefore in this study, we aimed to explore the biological role of ATP6V1H in osteogenic differentiation. OM (osteogenic medium) and HG (high glucose and free fatty acids) were used to induce the MC3T3-E1 cells into osteogenic differentiation in a T2DM simulating environment. CCK8 assay was used to detect cell viability. Alizarin Red staining was used to detect the influence of ATP6V1H on osteogenic differentiation. ATP6V1H expression increased in OM-MC3T3-E1 cells, while decreased in OM+HG-MC3T3-E1 cells. ATP6V1H promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. Overexpression of ATP6V1H inhibited Akt/GSK3β signaling pathway, while knockdown of ATP6V1H promoted Akt/GSK3β signaling pathway. ATP6V1H overexpression promoted osteogenic differentiation of OM+HG-MC3T3-E1 cells. The role of ATP6V1H in osteogenic differentiation in a T2DM simulating environment involved in Akt/GSK3β signaling pathway. These data demonstrated that ATP6V1H could serve as a potential target for osteogenic differentiation in a T2DM simulating environment.

Abstract Image

查看原文本刊更多论文

ATP6V1H通过Akt/GSK3β信号通路促进MC3T3-E1细胞成骨分化。

2型糖尿病(T2DM)约占糖尿病患者的90%，骨质疏松是T2DM的并发症之一。ATP6V1H (v型质子atp酶亚基H)在抑制骨质流失中发挥重要作用，但其在成骨分化中的作用尚不清楚。因此，在本研究中，我们旨在探讨ATP6V1H在成骨分化中的生物学作用。在T2DM模拟环境下，采用OM(成骨培养基)和HG(高糖和游离脂肪酸)诱导MC3T3-E1细胞成骨分化。CCK8法检测细胞活力。茜素红染色检测ATP6V1H对成骨分化的影响。ATP6V1H在OM- mc3t3 - e1细胞中表达升高，而在OM+HG-MC3T3-E1细胞中表达降低。ATP6V1H促进OM+HG-MC3T3-E1细胞成骨分化。ATP6V1H过表达抑制Akt/GSK3β信号通路，而ATP6V1H敲低促进Akt/GSK3β信号通路。ATP6V1H过表达促进OM+HG-MC3T3-E1细胞成骨分化。ATP6V1H在T2DM模拟环境中参与Akt/GSK3β信号通路的成骨分化中的作用。这些数据表明，ATP6V1H可以作为T2DM模拟环境中成骨分化的潜在靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Organogenesis BIOCHEMISTRY & MOLECULAR BIOLOGY-DEVELOPMENTAL BIOLOGY

CiteScore

4.10

自引率

4.30%

发文量

审稿时长

>12 weeks

期刊介绍： Organogenesis is a peer-reviewed journal, available in print and online, that publishes significant advances on all aspects of organ development. The journal covers organogenesis in all multi-cellular organisms and also includes research into tissue engineering, artificial organs and organ substitutes. The overriding criteria for publication in Organogenesis are originality, scientific merit and general interest. The audience of the journal consists primarily of researchers and advanced students of anatomy, developmental biology and tissue engineering. The emphasis of the journal is on experimental papers (full-length and brief communications), but it will also publish reviews, hypotheses and commentaries. The Editors encourage the submission of addenda, which are essentially auto-commentaries on significant research recently published elsewhere with additional insights, new interpretations or speculations on a relevant topic. If you have interesting data or an original hypothesis about organ development or artificial organs, please send a pre-submission inquiry to the Editor-in-Chief. You will normally receive a reply within days. All manuscripts will be subjected to peer review, and accepted manuscripts will be posted to the electronic site of the journal immediately and will appear in print at the earliest opportunity thereafter.