Autoimmunity最新文献

{"title":"MiR-300 promotes the proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis by targeting IL-37","authors":"Ying Wang, Ge Zhang, Wei Huang","doi":"10.1080/08916934.2022.2081842","DOIUrl":"https://doi.org/10.1080/08916934.2022.2081842","url":null,"abstract":"Abstract Background Fibroblast-like synoviocytes (FLS) are crucial regulators in the pathogenesis of rheumatoid arthritis (RA). Reportedly, microRNA (miR) participates in regulating the pathogenesis of RA. In this study, we explored the regulatory effects of miR-300 on the proliferation, migration and invasion of FLS, which were obtained from RA patients. Methods qPCR was utilized to detect miR-300 expression and interleukin-37 (IL-37) mRNA expression in the synovial tissue of RA patients and healthy controls. Cell counting kit-8 (CCK-8) assay and Transwell assay were performed to investigate the regulatory function of miR-300 on the proliferation, migration and invasion of FLS. ELISA was employed to detect TNF-α, IL-6 and IL-8 levels, to evaluate the inflammatory response. Bioinformatics analysis and luciferase reporter assay were applied to validate the targeting relationship between miR-300 and IL-37. Western blot assay was executed to detect IL-37 protein expression in FLS. Results MiR-300 was revealed to be markedly down-modulated in the synovial tissue and FLS of RA patients; meanwhile, IL-37 expression was up-modulated. The transfection of miR-300 mimics enhanced RA-FLS growth, migration, invasion and inflammatory response; transfection of miR-300 inhibitors repressed the growth, migration, invasion and inflammatory response of RA-FLS. IL-37 was identified as a downstream target of miR-300, and IL-37 partially counteracted the enhanced growth, migration, invasion and inflammatory response of RA-FLS induced by miR-300. Conclusion MiR-300 facilitates growth, migration, invasion and inflammatory response of FLS by targeting IL-37, suggesting it was a crucial regulator in the pathogenesis of RA.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"371 - 377"},"PeriodicalIF":3.5,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46498225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BML-111 alleviates inflammatory response of alveolar epithelial cells via miR-494/Slit2/Robo4 signalling axis to improve acute lung injury","authors":"F. Zou, Zhong-Bao Zhuang, Shuang-Shuang Zou, Bu Wang, Zhihua Zhang","doi":"10.1080/08916934.2022.2065671","DOIUrl":"https://doi.org/10.1080/08916934.2022.2065671","url":null,"abstract":"Abstract Acute lung injury (ALI) is a common, variously induced lung cell injury with high mortality. It is also an early stage of acute respiratory distress syndrome. BML-111 is a lipoxin A4 receptor agonist that plays an important role in inflammation. However, its function on ALI remains unclear. To explore whether BML-111 is involved in ALI and its regulatory molecular mechanism, we constructed an in vitro ALI model by stimulating primary mouse alveolar epithelial cells (AECs) with lipopolysaccharide (LPS). The downstream target of microRNA (miR)-494 was predicted by Targetscan. The apoptosis and expression of inflammatory cytokines were analysed by RT-qPCR, Western blot, and ELISA. BML-111 treatment alleviated LPS-induced apoptosis and the production of inflammatory cytokines, such as tumour necrosis factor α, interleukin (IL)-6, IL-1β, in primary mouse AECs via downregulating miR-494. MiR-494 targeted and downregulated slit guidance ligand 2 (Slit2) in primary mouse AECs. BML-111 activated the Slit2/roundabout guidance receptor 4 (Robo4) axis via downregulating miR-494 to reduce LPS-induced damage in AECs. This study elucidated that miR-494 on BML-111 alleviated LPS-induced ALI in primary mouse AECs via downregulating miR-494 and subsequently activating the Slit2/Robo4 axis. These findings provided a new idea for the prevention and treatment of ALI and respiratory distress syndrome.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"318 - 327"},"PeriodicalIF":3.5,"publicationDate":"2022-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47677418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0060531 knockdown ameliorates IL-22-induced keratinocyte damage by binding to miR-330-5p to decrease GAB1 expression.","authors":"Quan Shi, Jing Luo, Weiming Chen, Qi He, Jianwen Long, Bo Zhang","doi":"10.1080/08916934.2022.2037127","DOIUrl":"10.1080/08916934.2022.2037127","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is a chronic immune-mediated skin disease. Recent studies showed its pathogenesis involved circular RNA (circRNA). However, the role of circ_0060531 in psoriasis development and the behind mechanism remain to be explored.</p><p><strong>Methods: </strong>Psoriasis cell model was constructed by treating keratinocytes (HaCaT cells) using interleukin 22 (IL-22). Expression of circ_0060531, microRNA-330-5p (miR-330-5p) and GRB2 associated binder 1 (GAB1) was determined by quantitative real-time polymerase chain reaction. The functional effects of circ_0060531 on IL-22-caused cell injury were investigated by 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide, 5-Ethynyl-29-deoxyuridine, wound-healing and enzyme-linked immunosorbent assays. Protein expression was analysed by Western blot. The interactions among circ_0060531, miR-330-5p and GAB1 were identified by dual-luciferase reporter or RNA immunoprecipitation assay.</p><p><strong>Results: </strong>Circ_0060531 and GAB1 expression were significantly increased, while miR-330-5p was decreased in psoriatic skin biopsies and IL-22-stimulated HaCaT cells in comparison with controls. In function, circ_0060531 knockdown assuaged IL-22-induced cell proliferation, cell migration and inflammation. Besides, circ_0060531 acted as a miR-330-5p sponge, and regulated the processes of IL-22-treated HaCaT cells by binding to the miRNA. Under the treatment of IL-22, miR-330-5p mediated HaCaT cell damage by targeting GAB1. Importantly, circ_0060531 modulated GAB1 production by interacting with miR-330-5p.</p><p><strong>Conclusion: </strong>Circ_0060531 knockdown assuaged IL-22-induced keratinocyte dysfunction through miR-330-5p/GAB1 pathway, proving a novel target for the therapy of psoriasis.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"243-253"},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44034553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circ_0016347 modulates proliferation, migration, invasion, cell cycle, and apoptosis of osteosarcoma cells <i>via</i> the miR-661/IL6R axis.","authors":"Yan Liu,&nbsp;Jianjun Yuan,&nbsp;Quan Zhang,&nbsp;Zhishuai Ren,&nbsp;Guang Li,&nbsp;Rong Tian","doi":"10.1080/08916934.2022.2037129","DOIUrl":"https://doi.org/10.1080/08916934.2022.2037129","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma is a common primary bone tumour in children and adolescents. Circular RNAs (circRNAs) exert vital functions in human diseases, including osteosarcoma. Therefore, we explored the role of circ_0016347 in osteosarcoma.</p><p><strong>Methods: </strong>The real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of circ_0016347, microRNA-661 (miR-661), and Interleukin-6 receptor (IL6R) in osteosarcoma tissues and cells. The proliferation of osteosarcoma cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and EdU experiments. The migration and invasion were determined by transwell assay. The cell cycle distribution and apoptosis were assessed by flow cytometry assay. The association relationships among circ_0016347, miR-661, and IL6R were analyzed by dual-luciferase reporter assays. The western blot assay was employed to assay the protein expression. A xenograft experiment was established to clarify the functional role of circ_0016347 inhibition <i>in vivo</i>.</p><p><strong>Results: </strong>Circ_0016347 was obviously overexpressed in osteosarcoma tissues and cells compared with control groups. The suppression of circ_0016347 impeded proliferation, migration, invasion, and cell cycle and induced apoptosis in osteosarcoma cells, which was overturned by knockdown of miR-661. Consistently, circ_0016347 knockdown repressed tumour growth <i>in vivo</i>. Moreover, miR-661 directly targeted and inhibited IL6R, and the upregulation of IL6R reversed miR-661-induced effects on osteosarcoma cells. Furthermore, circ_0016347 could regulate IL6R expression through miR-661. Inhibition of circ_0016347 also inactivated the Janus kinase 2 (JAK2)/Transcription 3 (STAT3) signalling pathway in osteosarcoma cells by IL6R.</p><p><strong>Conclusion: </strong>Circ_0016347 functioned as an oncogene in osteosarcoma at least in part by the miR-661/IL6R axis and JAK2/STAT3 signalling pathway.</p>","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 4","pages":"264-274"},"PeriodicalIF":3.5,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39925714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-361-5p promotes proliferation and inhibits apoptosis of fibroblast-like synoviocytes via targeting ZBTB10 in rheumatoid arthritis","authors":"Aixian Zhang, R. Lu, H. Lang, Min Wu","doi":"10.1080/08916934.2022.2073588","DOIUrl":"https://doi.org/10.1080/08916934.2022.2073588","url":null,"abstract":"Abstract Objectives This study is aimed to explore the key role of miR-361-5p in fibroblast-like synovial (FLS) cells of rheumatoid arthritis (RA) and explore the underlying mechanism. Methods First, we performed RT-qPCR to evaluate the expression of miR-361-5p in both synovial tissues of RA patients and cultured RA-FLS cells. Then CCK-8 assay, EdU staining, Western blot, flow cytometry, and ELISA were conducted to estimate the influence of inhibiting miR-361-5p on RA-FLS cells. Moreover, we used bioinformatics analysis to predict the potential targets of miR-361-5p and perform a dual luciferase report assay for verification. Finally, rescue experiments were performed to prove the role of miR-361-5p/Zinc Finger And BTB Domain Containing 10 (ZBTB10) in the proliferation, cell cycle, and apoptosis of RA-FLS. Results We find that the expression of miR-361-5p is increased in both RA tissues and cultured RA-FLS cells. The inhibition of miR-361-5p can not only inhibit proliferation, arrest the cell cycle in G1/G0 phase, and increase apoptosis, but also reduce the inflammatory factors secreted by RA-FLS cells. In addition, ZBTB10 is a direct target for miR-361-5p, over-expression of ZBTB10 reverses the effect of miR-361-5p in RA-FLS. Conclusions MiR-361-5p promotes the progression of rheumatoid arthritis by targeting ZBTB10. Key points The influences of miR-361-5p on RA-FLS cells.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"310 - 317"},"PeriodicalIF":3.5,"publicationDate":"2022-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48576073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA LINC00707 serves as a sponge of miR-382-5p to alleviate lipopolysaccharide (LPS)-induced WI-38 cell injury through upregulating NKAP in infantile pneumonia","authors":"Lu Chen, Yanping Chen, Jian-Bao Huang, Ji-Yan Zhang","doi":"10.1080/08916934.2022.2062594","DOIUrl":"https://doi.org/10.1080/08916934.2022.2062594","url":null,"abstract":"Abstract Infantile pneumonia (IP) is an acute lower respiratory infection that imposes a heavy burden on children’s health. Increasing evidence has demonstrated that long non-coding RNA (lncRNA) LINC00707 participates in the regulation of the pneumonia process. Cell proliferative ability and apoptosis were measured using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2’-deoxyuridine (EdU), and flow cytometry assays. Bcl-2 related X protein (Bax), NF-kB activating protein (NKAP), p-P65, P65, p-IκBα, and IκBα protein levels were detected using western blot assay. The binding between miR-382-5p and LINC00707 or NKAP was predicted by starBase v2.0 and then verified by a dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. LINC00707 and NKAP levels were increased, and miR-382-5p was decreased in LPS-stimulated WI-38 cells. Furthermore, the silencing of LINC00707 could abrogate LPS-engendered WI-38 cell proliferation, apoptosis, and oxidative stress. LINC00707 deficiency could relieve LPS-triggered WI-38 cell damage by regulating the miR-382-5p/NKAP axis, providing a new therapeutic strategy for IP treatment.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"328 - 338"},"PeriodicalIF":3.5,"publicationDate":"2022-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41346260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between IL-23R gene polymorphism (rs10889677 A/C) and ankylosing spondylitis and rheumatoid arthritis susceptibility: A meta-analysis with trial sequential analysis","authors":"Zhang Tao, Lingxiang Yu, Ming Shao, Ye Wu, Jinian Wang, Y. Deng, M. Ni, Xiaoya Sun, Yuting Chen, Shanshan Xu, Yubo Ma, Z. Shuai, F. Pan","doi":"10.1080/08916934.2022.2076837","DOIUrl":"https://doi.org/10.1080/08916934.2022.2076837","url":null,"abstract":"Abstract Objectives Autoimmune diseases are a kind of chronic diseases for which the immune system loses tolerance to autoantigens. This meta-analysis’ purpose is to determine whether there exists a correlation between IL-23R polymorphism and common autoimmune diseases like ankylosing spondylitis (AS) and rheumatoid arthritis (RA). Methods We searched the relevant literatures up to September 2021 and used different effect models for meta-analysis. 95% confidence interval (95% CI) and odds ratio (OR) were used to determine the relationship between rs10889677 (A/C) polymorphism and AS as well as RA. Finally, to promote the reliability of results, the trial sequential analysis (TSA) has also been applied and we searched the data related to autoimmune diseases (AS, RA) on genome-wide association studies (GWAS). Results Generally, 31 studies were included. Rs10889677 (A/C) was significantly correlated with the susceptibility to AS and RA among the general individuals (p < .05). Moreover, there existed a relevance between allele A and AS as well as RA in Caucasians (p < .05). AA genotype increased the risk of autoimmune diseases in Mongolians. As a result, the robustness of meta-analysis has further been proved by TSA. Conclusion IL-23R (rs10889677 A/C) A allele was a risk gene for AS and RA in the general population, especially in Caucasians. AA genotype increased the risk of AS and RA in Mongolians.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"388 - 397"},"PeriodicalIF":3.5,"publicationDate":"2022-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42942298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of SAA1 as a prognostic biomarker associated with immune infiltration in glioblastoma","authors":"Gang Cui, Youchao Xiao","doi":"10.1080/08916934.2022.2076085","DOIUrl":"https://doi.org/10.1080/08916934.2022.2076085","url":null,"abstract":"Abstract Glioblastoma (GBM) is the most lethal tumour in the central nervous system (CNS), GBM has a poor prognosis due to treatment tolerance and tumour recurrence; new molecular biomarkers are needed to acquire accurate prognosis and to promote therapeutic strategies. Data from Gene Expression Omnibus (GEO) was analysed to screen differentially expressed genes (DEGs), and 279 DEGs were screened. The protein–protein interaction (PPI) network of DEGs was constructed and visualized, top 10 hub genes were identified by using Cytoscape consequently. The function of DEGs was explored by enrichment analysis, DEGs were enriched in tumour-associated biologic processions and pathways. Gene Expression Profiling Interactive Analysis (GEPIA) database was used to identify prognostic genes; serum amyloid A1 (SAA1) was identified as a critical prognostic gene due to higher SAA1 expression associated with poor overall survival (OS) (HR = 1.5, p < .05) and poor disease-free survival (DFS) (HR = 1.9, p < .01). Dataset from The Chinese Glioma Genome Atlas database validated the prognostic value of SAA1 and reported the relationship between SAA1 expression and clinical characteristics, including age, sex, history of relapse, and the status of IDH. Gene set enrichment analysis (GSEA) identified six SAA1-related pathways; the identification of pathways could provide insight into the therapeutic strategies of GBM. Lastly, the relationship between SAA1 expression and immune infiltration was explored, and the result showed that SAA1 expression negatively correlated with the infiltration level of T cells, and SAA1 expression positively correlated with the infiltration level of Treg cells. The overexpression of SAA1 was associated with poor OS and DFS in GBM, and the expression of the SAA1 gene may affect the infiltration level of immune cells. Therefore, SAA1 could be a promising prognostic biomarker associated with immune infiltration and therapeutic target for GBM.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"418 - 427"},"PeriodicalIF":3.5,"publicationDate":"2022-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49502140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium propionate improves rheumatoid arthritis by inhibiting survivin mediated proliferation of fibroblast like synoviocytes by promoting miR-140-5p","authors":"Sha Ma, Jing Wang, Fang He, Dachen Zuo, Fayou Li, H. Fan, Z. Yin, H. Liang, Qin Li","doi":"10.1080/08916934.2022.2073589","DOIUrl":"https://doi.org/10.1080/08916934.2022.2073589","url":null,"abstract":"Abstract Background Increased proliferation and impaired death of fibroblast-like synovial cells play an important role in the development of rheumatoid arthritis (RA). Survivin plays an important role in the prodromal stage and prognosis of RA and has been introduced as a biomarker of joint injury in RA patients. The purpose of this study was to explore whether propionate alleviates RA through miR-140-5p/survivin pathway. Methods The synovial tissues of RA patients were collected to detect the expression levels of miR-140-5p and survivin; normal human fibroblast-like synovial cells (HLSs) and RA fibroblast-like synovial cells (RA-FLSs) were cultured and treated with 10 mM of sodium propionate (SP), then the expressions of miR-140-5p and survivin, cell viability and apoptosis were detected; collagen induced arthritis (CIA) rat model was constructed and treated with SP, then the tissue inflammation level and the expression levels of miR-140-5p and Survivin were detected. Results The expression of miR-140-5p decreased in synovial tissues of RA patients and RA-FLSs cells, while the expression of survivin increased significantly in RA patients. SP promoted miR-140-5p expression and apoptosis in RA-FLSs cells and inhibited survivin expression and cell viability of RA-FLSs cells. In addition, miR-140-5p plays a protective role by targeting survivin. Importantly, in the CIA rat model, SP reduced joint inflammatory response, and the miR-140-5p inhibitor weakened the protective effect of SP. Conclusion SP can alleviate RA by promoting the expression of miR-140-5p and inhibiting the excessive proliferation and death impairment of RA-FLSs cells induced by survivin.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"378 - 387"},"PeriodicalIF":3.5,"publicationDate":"2022-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44542038","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel circRNA, circRACGAP1, hampers the progression of systemic lupus erythematosus via miR-22-3p-mediated AKT signalling","authors":"Han-Ying Mei, Ju Liu, Xiao-Ping Shen, R. Wu","doi":"10.1080/08916934.2022.2073590","DOIUrl":"https://doi.org/10.1080/08916934.2022.2073590","url":null,"abstract":"Abstract Background Systemic lupus erythematosus (SLE) is defined as a multisystem autoimmune disease involving various organs, of which exact molecular mechanisms remain elusive. Here, we aimed to investigate a novel circular RNA (circRNA), circRACGAP1, abnormally expressed in SLE and explored its underlying regulatory network. Methods The expression patterns of circRACGAP1 were determined in patients diagnosed with SLE by using a qRT-PCR assay. Spearman correlation analysis was employed to evaluate the correlation between circRACGAP1 and clinicopathological variables in patients with SLE. Flow cytometry and TUNEL assays were subjected to assess the cell apoptosis. Nuclear-cytoplasmic fractionation and luciferase reporter assay was used to verify the circRACGAP1/miR-22-3p/PTEN axis. Western blot analysis was performed to measure the PTEN/AKT signalling-related proteins and apoptotic-related biomarkers. Results Down-regulated circRACGAP1 was observed and correlated with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) score, anti-double-stranded (ds) DNA, and complement C3 level in patients with SLE. Overexpression of circRACGAP1 significantly alleviated cell apoptosis in Jurkat cells within UVB exposure. Mechanistic investigation revealed that circRACGAP1 could serve as a sponge of miR-22-3p to regulate PTEN/AKT signalling. Conclusions Collectively, circRACGAP1 regulated the AKT signalling pathway via binding to miR-22-3p in the progression of SLE, suggesting therapeutic targets for SLE treatment.","PeriodicalId":8688,"journal":{"name":"Autoimmunity","volume":"55 1","pages":"360 - 370"},"PeriodicalIF":3.5,"publicationDate":"2022-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45159713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}