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FRZB通过调节Wnt/β-连环蛋白信号通路影响金黄色葡萄球菌诱导的人骨髓源干细胞骨髓炎。

FRZB affects aureus‑induced osteomyelitis in human bone marrow derived stem cells by regulating the Wnt/β‑catenin signaling pathway.

作者信息

Li Xin, Pang Wenyong, Fan Hongsong, Wang Hao, Zhang Leibing

机构信息

Department of Emergency Surgery, Guizhou Provincial People's Hospital, Guiyang, Guizhou 550023, P.R. China.

出版信息

Exp Ther Med. 2023 Sep 28;26(5):531. doi: 10.3892/etm.2023.12230. eCollection 2023 Nov.

DOI:10.3892/etm.2023.12230
PMID:37869648
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10587868/
Abstract

Osteomyelitis is an infectious disease of bone tissue caused by bacterial infection, which can infect through hematogenous, traumatic or secondary ways and then lead to acute or chronic bone injury and relative clinical symptoms, bringing physical injury and economic burden to patients. Frizzled related protein (FRZB) participates in the regulation of various diseases (osteoarthritis, cardiovascular diseases and types of cancer) by regulating cell proliferation, motility, differentiation and inflammation, while its function in osteomyelitis remains to be elucidated. The present study aimed to uncover the role and underlying mechanism of FRZB mediation in ()-induced osteomyelitis. Human bone marrow derived stem cells (hBMSCs) were treated with to imitate an inflammatory osteomyelitis micro-environment , then mRNA and protein expression were severally assessed by RT-PCR and western blotting. The activity, apoptosis and differentiation of the cells were characterized via CCK-8, caspase-3 activity and Alizarin red sulfate/alkaline phosphatase staining, respectively. Expression levels of FRZB were upregulated in . -infected hBMSCs. Over-expression of FRZB significantly reduced hBMSC cell viability and differentiation while promoting cell apoptosis with or without . infection. However, FRZB knockdown reversed these effects. Once Wnt was impeded, the effect of FRZB downregulation was impeded to a great extent. Taken together, FRZB participated to regulate the osteomyelitis by activating the Wnt/β-catenin signaling pathway.

摘要

骨髓炎是一种由细菌感染引起的骨组织感染性疾病,可通过血行、创伤或继发途径感染,进而导致急性或慢性骨损伤及相关临床症状,给患者带来身体伤害和经济负担。卷曲相关蛋白(FRZB)通过调节细胞增殖、运动、分化和炎症参与多种疾病(骨关节炎、心血管疾病和各类癌症)的调控,而其在骨髓炎中的作用尚待阐明。本研究旨在揭示FRZB在()诱导的骨髓炎中的作用及潜在机制。用人骨髓来源的干细胞(hBMSCs)进行处理以模拟炎性骨髓炎微环境,然后分别通过逆转录聚合酶链反应(RT-PCR)和蛋白质印迹法评估mRNA和蛋白质表达。分别通过CCK-8、半胱天冬酶-3活性和茜素红硫酸盐/碱性磷酸酶染色来表征细胞的活性、凋亡和分化。在()感染的hBMSCs中,FRZB的表达水平上调。无论有无()感染,FRZB的过表达均显著降低hBMSC细胞活力和分化,同时促进细胞凋亡。然而,FRZB基因敲低可逆转这些效应。一旦Wnt被阻断,FRZB下调的作用在很大程度上受到阻碍。综上所述,FRZB通过激活Wnt/β-连环蛋白信号通路参与调节骨髓炎。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/701eafb8fbd5/etm-26-05-12230-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/300155809384/etm-26-05-12230-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/327b77d6812a/etm-26-05-12230-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/9ee642cb213a/etm-26-05-12230-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/05fd03cd55a9/etm-26-05-12230-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/468f1d5d731a/etm-26-05-12230-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/701eafb8fbd5/etm-26-05-12230-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/300155809384/etm-26-05-12230-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/327b77d6812a/etm-26-05-12230-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/9ee642cb213a/etm-26-05-12230-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/05fd03cd55a9/etm-26-05-12230-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/468f1d5d731a/etm-26-05-12230-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e73/10587868/701eafb8fbd5/etm-26-05-12230-g05.jpg

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