Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat.
Qing Fan, Zhu Liu, Chao Shen, Hai Li, Jing Ding, Fangchun Jin, Lin Sha, Ziming Zhang
{"title":"Microarray study of gene expression profile to identify new candidate genes involved in the molecular mechanism of leptin-induced knee joint osteoarthritis in rat.","authors":"Qing Fan, Zhu Liu, Chao Shen, Hai Li, Jing Ding, Fangchun Jin, Lin Sha, Ziming Zhang","doi":"10.1186/s41065-017-0039-z","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA) is one of the most prevalent chronic joint diseases while the precise genetic mechanism remains elusive. In this study, we investigated the gene expression profile in OA by microarray analysis.</p><p><strong>Results: </strong>Histopathological characteristics of OA cartilage were examined using a rat model of leptin-induced OA. Gene expression profile of leptin-induced articular cartilage and healthy rat cartilage were compared using genome-wide microarray hybridization. A total of 1857 genes differentially expressed genes (1197 upregulated and 660 downregulated) were identified, some of which are known to be associated with leptin-induced OA phenotype. These included genes related to MMPs, inflammatory factors, growth factors, apoptotic genes and osteogenic genes. In addition, upregulated expressions of some new candidate genes, which have hitherto fore not been linked to OA (such as <i>BCL2L11</i>) were detected in leptin-induced OA cartilage, which suggests that these genes might be important for OA molecular mechanism.</p><p><strong>Conclusion: </strong>Our findings suggest that pathogenesis of leptin-induced OA involves modulation of expression of multiple genes, although the underlying molecular mechanisms need to be studied further. Further investigation of leptin-induced gene expression changes is needed to gain new insights into the molecular mechanism of OA pathogenesis.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2017-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/s41065-017-0039-z","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s41065-017-0039-z","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2018/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 10
Abstract
Background: Osteoarthritis (OA) is one of the most prevalent chronic joint diseases while the precise genetic mechanism remains elusive. In this study, we investigated the gene expression profile in OA by microarray analysis.
Results: Histopathological characteristics of OA cartilage were examined using a rat model of leptin-induced OA. Gene expression profile of leptin-induced articular cartilage and healthy rat cartilage were compared using genome-wide microarray hybridization. A total of 1857 genes differentially expressed genes (1197 upregulated and 660 downregulated) were identified, some of which are known to be associated with leptin-induced OA phenotype. These included genes related to MMPs, inflammatory factors, growth factors, apoptotic genes and osteogenic genes. In addition, upregulated expressions of some new candidate genes, which have hitherto fore not been linked to OA (such as BCL2L11) were detected in leptin-induced OA cartilage, which suggests that these genes might be important for OA molecular mechanism.
Conclusion: Our findings suggest that pathogenesis of leptin-induced OA involves modulation of expression of multiple genes, although the underlying molecular mechanisms need to be studied further. Further investigation of leptin-induced gene expression changes is needed to gain new insights into the molecular mechanism of OA pathogenesis.