{"title":"LncRNA SNHG7通过海绵miR-146b抑制IL-β诱导的骨关节炎细胞凋亡和增殖。","authors":"Naikai Lin, Zehui Song, Bitao Ma, Peng Wang","doi":"10.1080/03008207.2025.2487470","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>We probed the roles of SNHG7, miR-146b, PCBP1, and IL-β in the development of osteoarthritis (OA).</p><p><strong>Materials and methods: </strong>OA models were established using anterior cruciate ligaments, and chondrocytes were obtained from mouse cartilage tissue. Cells were treated with 10 ng/ml Il-1β. RT-qPCR was used to detect the expression of SNHG7, miR-146b, PCBP1, and IL-β in tissues and cells. Safranin-O/Fast Green staining was performed to analyze the cartilage damage in each group of mice.</p><p><strong>Results: </strong>SNHG7 and PCBP1 expressions were down-regulated, and miR-146b expression was up-regulated in OA tissue and IL-1β-treated chondrocytes compared to normal cartilage tissue and chondrocytes. Forced SNHG7 expression improved cartilage structure, enhanced proliferative viability of chondrocytes, and inhibited apoptosis and IL-1β release in IL-1β-treated chondrocytes in OA mice. In contrast, miR-146b upregulation decreased proliferative viability and promoted apoptosis and IL-1β release in chondrocytes. Rescue assays showed that miR-146b attenuated the protective effects of SNHG7 on apoptosis and inflammation in IL-1β-treated chondrocytes, and activation of PCBP1 expression significantly inhibited the cytotoxic effects of miR-146b. Mechanistically, SNHG7 acted as a competitive endogenous RNA by targeting miR-146b to promote the expression of PCBP1.</p><p><strong>Conclusions: </strong>This study confirms that SNHG7 inhibits IL-1β-mediated inflammatory responses in chondrocytes via the miR-146b/PCBP1 axis, thereby suppressing IL-1β-induced OA.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":" ","pages":"1-14"},"PeriodicalIF":2.8000,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA SNHG7 inhibits apoptosis and proliferation of osteoarthritis cells induced by IL-β through sponging miR-146b.\",\"authors\":\"Naikai Lin, Zehui Song, Bitao Ma, Peng Wang\",\"doi\":\"10.1080/03008207.2025.2487470\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>We probed the roles of SNHG7, miR-146b, PCBP1, and IL-β in the development of osteoarthritis (OA).</p><p><strong>Materials and methods: </strong>OA models were established using anterior cruciate ligaments, and chondrocytes were obtained from mouse cartilage tissue. Cells were treated with 10 ng/ml Il-1β. RT-qPCR was used to detect the expression of SNHG7, miR-146b, PCBP1, and IL-β in tissues and cells. Safranin-O/Fast Green staining was performed to analyze the cartilage damage in each group of mice.</p><p><strong>Results: </strong>SNHG7 and PCBP1 expressions were down-regulated, and miR-146b expression was up-regulated in OA tissue and IL-1β-treated chondrocytes compared to normal cartilage tissue and chondrocytes. Forced SNHG7 expression improved cartilage structure, enhanced proliferative viability of chondrocytes, and inhibited apoptosis and IL-1β release in IL-1β-treated chondrocytes in OA mice. In contrast, miR-146b upregulation decreased proliferative viability and promoted apoptosis and IL-1β release in chondrocytes. Rescue assays showed that miR-146b attenuated the protective effects of SNHG7 on apoptosis and inflammation in IL-1β-treated chondrocytes, and activation of PCBP1 expression significantly inhibited the cytotoxic effects of miR-146b. Mechanistically, SNHG7 acted as a competitive endogenous RNA by targeting miR-146b to promote the expression of PCBP1.</p><p><strong>Conclusions: </strong>This study confirms that SNHG7 inhibits IL-1β-mediated inflammatory responses in chondrocytes via the miR-146b/PCBP1 axis, thereby suppressing IL-1β-induced OA.</p>\",\"PeriodicalId\":10661,\"journal\":{\"name\":\"Connective Tissue Research\",\"volume\":\" \",\"pages\":\"1-14\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-04-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Connective Tissue Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/03008207.2025.2487470\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Connective Tissue Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/03008207.2025.2487470","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
目的:探讨SNHG7、miR-146b、PCBP1和IL-β在骨关节炎(OA)发生中的作用。材料和方法:采用前交叉韧带建立骨关节炎模型,小鼠软骨组织制备软骨细胞。细胞用10 ng/ml Il-1β处理。RT-qPCR检测组织和细胞中SNHG7、miR-146b、PCBP1、IL-β的表达。采用红素- o /Fast Green染色法分析各组小鼠软骨损伤情况。结果:与正常软骨组织和软骨细胞相比,OA组织和il -1β处理的软骨细胞中SNHG7和PCBP1的表达下调,miR-146b的表达上调。强迫SNHG7表达改善OA小鼠软骨结构,增强软骨细胞增殖活力,抑制IL-1β处理的软骨细胞凋亡和IL-1β释放。相反,miR-146b上调降低了软骨细胞的增殖活力,促进了细胞凋亡和IL-1β的释放。救援实验显示,miR-146b减弱了SNHG7对il -1β处理的软骨细胞凋亡和炎症的保护作用,激活PCBP1表达可显著抑制miR-146b的细胞毒性作用。机制上,SNHG7作为竞争性内源性RNA,靶向miR-146b促进PCBP1的表达。结论:本研究证实SNHG7通过miR-146b/PCBP1轴抑制il -1β介导的软骨细胞炎症反应,从而抑制il -1β诱导的OA。
LncRNA SNHG7 inhibits apoptosis and proliferation of osteoarthritis cells induced by IL-β through sponging miR-146b.
Purpose: We probed the roles of SNHG7, miR-146b, PCBP1, and IL-β in the development of osteoarthritis (OA).
Materials and methods: OA models were established using anterior cruciate ligaments, and chondrocytes were obtained from mouse cartilage tissue. Cells were treated with 10 ng/ml Il-1β. RT-qPCR was used to detect the expression of SNHG7, miR-146b, PCBP1, and IL-β in tissues and cells. Safranin-O/Fast Green staining was performed to analyze the cartilage damage in each group of mice.
Results: SNHG7 and PCBP1 expressions were down-regulated, and miR-146b expression was up-regulated in OA tissue and IL-1β-treated chondrocytes compared to normal cartilage tissue and chondrocytes. Forced SNHG7 expression improved cartilage structure, enhanced proliferative viability of chondrocytes, and inhibited apoptosis and IL-1β release in IL-1β-treated chondrocytes in OA mice. In contrast, miR-146b upregulation decreased proliferative viability and promoted apoptosis and IL-1β release in chondrocytes. Rescue assays showed that miR-146b attenuated the protective effects of SNHG7 on apoptosis and inflammation in IL-1β-treated chondrocytes, and activation of PCBP1 expression significantly inhibited the cytotoxic effects of miR-146b. Mechanistically, SNHG7 acted as a competitive endogenous RNA by targeting miR-146b to promote the expression of PCBP1.
Conclusions: This study confirms that SNHG7 inhibits IL-1β-mediated inflammatory responses in chondrocytes via the miR-146b/PCBP1 axis, thereby suppressing IL-1β-induced OA.
期刊介绍:
The aim of Connective Tissue Research is to present original and significant research in all basic areas of connective tissue and matrix biology.
The journal also provides topical reviews and, on occasion, the proceedings of conferences in areas of special interest at which original work is presented.
The journal supports an interdisciplinary approach; we present a variety of perspectives from different disciplines, including
Biochemistry
Cell and Molecular Biology
Immunology
Structural Biology
Biophysics
Biomechanics
Regenerative Medicine
The interests of the Editorial Board are to understand, mechanistically, the structure-function relationships in connective tissue extracellular matrix, and its associated cells, through interpretation of sophisticated experimentation using state-of-the-art technologies that include molecular genetics, imaging, immunology, biomechanics and tissue engineering.