The Influence of Zoledronic Acid on the Proliferation and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells and Tibial Fracture in Rats via Phosphatidylinositol-3-Kinase/AKT Pathway

IF 0.1 4区医学 Journal of Biomaterials and Tissue Engineering Pub Date : 2023-02-01 DOI:10.1166/jbt.2023.3258

Jianzhou Liu, Hao Wang, GuoJun Shang, Xiangyang Lv, Zhenwei Xu, Fujun Xiong

{"title":"The Influence of Zoledronic Acid on the Proliferation and Osteogenic Differentiation of Bone Marrow Mesenchymal Stem Cells and Tibial Fracture in Rats via Phosphatidylinositol-3-Kinase/AKT Pathway","authors":"Jianzhou Liu, Hao Wang, GuoJun Shang, Xiangyang Lv, Zhenwei Xu, Fujun Xiong","doi":"10.1166/jbt.2023.3258","DOIUrl":null,"url":null,"abstract":"Fracture healing is an extremely complex physiological process, involving a sequence of crucial mechanisms. Whether zoledronic acid (ZA) affects proliferation and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and tibial fractures still remains unknown. We\n performed construction of the tibial fracture model in rats and analyzed the impact of ZA and ZA+LY294002 on fracture healing in rats. Test of the influence of ZA and ZA+LY294002 on crucial osteogenic genes alkaline phosphatase (ALP), RUNX2, OCN and OPN was performed. Examination of the influence\n of suppressing the PI3K/AKT pathway on the proliferation with bone differentiation of ZA. Results showed ZA distinctly accelerated the proliferation and ALP activity of BMSC cells, BMP2, RUNX2, OCN, OPN and the activation of the PI3K/AKT pathway. Repression of PI3K/AKT pathway suppressed the\n proliferation and osteogenic differentiation action of ZA. ZA boosted tibial fracture healing in rats via activating the PI3K/AKT pathway. ZA facilitates the proliferation with osteogenic differentiation of BMSC cells and tibial fracture healing in rats via activating the PI3K/AKT pathway.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.3258","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 0

Abstract

Fracture healing is an extremely complex physiological process, involving a sequence of crucial mechanisms. Whether zoledronic acid (ZA) affects proliferation and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and tibial fractures still remains unknown. We performed construction of the tibial fracture model in rats and analyzed the impact of ZA and ZA+LY294002 on fracture healing in rats. Test of the influence of ZA and ZA+LY294002 on crucial osteogenic genes alkaline phosphatase (ALP), RUNX2, OCN and OPN was performed. Examination of the influence of suppressing the PI3K/AKT pathway on the proliferation with bone differentiation of ZA. Results showed ZA distinctly accelerated the proliferation and ALP activity of BMSC cells, BMP2, RUNX2, OCN, OPN and the activation of the PI3K/AKT pathway. Repression of PI3K/AKT pathway suppressed the proliferation and osteogenic differentiation action of ZA. ZA boosted tibial fracture healing in rats via activating the PI3K/AKT pathway. ZA facilitates the proliferation with osteogenic differentiation of BMSC cells and tibial fracture healing in rats via activating the PI3K/AKT pathway.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

唑来膦酸通过磷脂酰肌醇-3激酶/AKT通路对大鼠骨髓间充质干细胞增殖、成骨分化及胫骨骨折的影响

骨折愈合是一个极其复杂的生理过程，涉及一系列关键机制。唑来膦酸（ZA）是否影响骨髓间充质干细胞（BMSCs）的增殖和成骨分化以及胫骨骨折仍不清楚。我们构建了大鼠胫骨骨折模型，并分析了ZA和ZA+LY294002对大鼠骨折愈合的影响。试验ZA和ZA+LY294002对关键成骨基因碱性磷酸酶（ALP）、RUNX2、OCN和OPN的影响。研究了抑制PI3K/AKT通路对ZA增殖和骨分化的影响。结果表明，ZA明显加速了BMSC细胞、BMP2、RUNX2、OCN、OPN的增殖和ALP活性，并激活了PI3K/AKT通路。PI3K/AKT通路的抑制抑制了ZA的增殖和成骨分化作用。ZA通过激活PI3K/AKT通路促进大鼠胫骨骨折愈合。ZA通过激活PI3K/AKT途径促进BMSC细胞的增殖和成骨分化以及大鼠胫骨骨折愈合。

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分钟内获得全文去求助

来源期刊