Mechanism of Inflammatory Response Induced by Long Non-coding RNA LINC02863 Cooperates with MARK2 in the Pro-gression of Chronic Renal Failure

AERPATI Abulitibu; WANG Shun; ZHANG Li; HAN Yuanyuan; MUFUNAYI Aierken; MAO Zhijie; KANG Shao-tao; LIU Xinpeng

doi:10.13730/j.issn.2097-2148.2025.02.003

Abstract：Objective To investigate the mechanism of long non-coding RNA(lncRNA)LINC02863 cooperates with microtubule affinity-regulating kinase 2(MARK2)inducing inflammatory responses in the progression of chronic re-nal failure(CRF).Methods A cell model of CRF was established using HK-2 cells.After cell transfection,the cells were divided into the following groups:positive control group(CRF model cells),LINC02863 overexpression group(CRF model cells+LINC02863 overexpression gene)and LINC02863 silencing group(CRF model cells+LINC02863 silencing gene),the negative control group consisted of HK-2 cells cultured under normal oxygen conditions.The expressions of LINC02863 and MARK2 were measured by reverse transcription polymerase chain reaction(RT-PCR);cell viability was assessed using the cell counting kit 8(CCK-8)assay;apoptosis rates were detected by flow cytometry;creatinine and u-rea nitrogen expressions were measured by enzyme-linked immunosorbent assay(ELISA).The expressions of inflammatory factors such as tumor necrosis factor alpha(TNF-α)and interleukin 6(IL-6)were determined by RT-PCR,the expressions of MARK2,nuclear factor kap-pa B(NF-κB),interleukin 1 beta(IL-1β)and p65 pro-teins were assessed by Western blot.Results Compared with the negative control group,the positive control group showed significantly higher expression of LINC02863 and MARK2,increased cell apoptosis rate,elevated levels of creati-nine,urea nitrogen,TNF-α,IL-6 as well as higher protein expressions of MARK2,NF-κB,IL-1β and p65,cell viability was significantly reduced(all P＜0.05);after overexpressing LINC02863,the LINC02863 overexpression group exhibi-ted significantly higher levels of LINC02863,MARK2 gene expression,cell apoptosis,creatinine,urea nitrogen,TNF-α,IL-6,and protein levels of MARK2,NF-κB,IL-1β and p65 compared to the positive control group,while cell viability significantly decreased(all P＜0.05).After silencing LINC02863,the LINC02863 silencing group showed significantly lower levels of LINC02863 and MARK2 gene expression,reduced apoptosis rate,and lower levels of creatinine,urea ni-trogen,TNF-α,IL-6 and protein expressions of MARK2,NF-κB,IL-1β and p65,along with a significant increase in cell viability compared to the positive control group(all P＜0.05).Conclusion lncRNAs LINC02863 and MARK2 are aber-rantly upregulated in CRF.Overexpression of LINC02863 enhances the expression of MARK2 and promotes inflamma-tion,while silencing LINC02863 reduces MARK2 expression and alleviates the inflammatory response,improving CRF symptoms.These findings warrant further clinical investigation and potential application.