Knockdown of circ-FANCA alleviates LPS-induced HK2 cell injury via targeting miR-93-5p/OXSR1 axis in septic acute kidney injury

Li, Heyun; Zhang, Xia; Wang, Peng; Zhou, Xiaoyan; Liang, Haiying; Li, Caoni

doi:10.1186/s13098-021-00625-8

Cited by 50 publications

(50 citation statements)

References 40 publications

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“…CircRNAs have been demonstrated to compete with mRNAs for miRNAs binding, which inhibit downstream gene expression 30 . The biological functions of circRNA/miRNA/mRNA axis in sepsis have been revealed 31,32 . More importantly, bioinformatics analysis predicted the complementarity between miR‐17‐5p and circTLK1/PARP1.…”

Section: Introductionmentioning

confidence: 99%

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

Qiu

Qin

et al. 2021

J Cellular Molecular Medi

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Introduction Septic cardiomyopathy is a common complication of sepsis with high morbidity and mortality, but lacks specific therapy. This study aimed to reveal the role of circTLK1 and its potential mechanisms in septic cardiomyopathy. Materials and Methods The in vitro and in vivo models of septic cardiomyopathy were established. Cell viability and apoptosis were detected by CCK8, TUNEL and flow cytometry, respectively. LDH, CK, SOD, MDA, ATP, 8‐OHdG, NAD+/NADH ratio, ROS level, mitochondrial membrane potential and cytochrome C distribution were evaluated using commercial kits. qRT‐PCR and western blotting were performed to detect RNA and protein levels. Mitochondrial DNA (mtDNA) copy number and transcription were assessed by quantitative PCR. Dual‐luciferase assay, RNA immunoprecipitation and co‐immunoprecipitation were performed to verify the interaction between circTLK1/PARP1 and miR‐17‐5p. Results CircTLK1, PARP1 and HMGB1 were up‐regulated in the in vitro and in vivo models of septic cardiomyopathy. CircTLK1 inhibition restrained LPS‐induced up‐regulation of PARP1 and HMGB1. Moreover, circTLK1 knockdown repressed sepsis‐induced mtDNA oxidative damage, mitochondrial dysfunction and consequent cardiomyocyte apoptosis by inhibiting PARP1/HMGB1 axis in vitro and in vivo. In addition, circTLK1 enhanced PARP1 expression via sponging miR‐17‐5p. Inhibition of miR‐17‐5p abolished the protective effects of circTLK1 silencing on oxidative mtDNA damage and cardiomyocyte apoptosis. Conclusion CircTLK1 sponged miR‐17‐5p to aggravate mtDNA oxidative damage, mitochondrial dysfunction and cardiomyocyte apoptosis via activating PARP1/HMGB1 axis during sepsis, indicating that circTLK1 may be a putative therapeutic target for septic cardiomyopathy.

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Section: Introductionmentioning

confidence: 99%

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

Qiu

Qin

et al. 2021

J Cellular Molecular Medi

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“…OXSR1 is a serine/threonine kinase that regulates downstream kinases in response to environmental stress and is responsible for the co-transportation of ions in kidney [ 47 ]. Previous research revealed that OXSR1 level was higher in the serum of sepsis-related AKI patients compared to healthy individuals, and OXSR1 protein expression was strongly enhanced in LPS-stimulated HK2 cells compared to control cells [ 48 ]. In this study, OXSR1 expression was lifted in LPS-challenged cells and CLP-induced rats, which was in line with previous findings.…”

Section: Discussionmentioning

confidence: 99%

Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis in vitro and in vivo

Cui

Ren

et al. 2022

Renal Failure

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“…CXCL10 [76], SIGLEC1 [77] and IL1R2 [78] have been suggested to be associated with neurological diseases. CXCL9 [79], SIGLEC1 [80], IL1R2 [81], KLF15 [82] and CD207 [83] [146], STAT4 [147], CXCL8 [148], KLF2 [149], ADM (adrenomedullin) [150], EGR1 [151], TRIB1 [152], SOD2 [153], OXSR1 [154], IL6R [155], CD44 [156], LRG1 [157], PFKFB2 [158], PACSIN2 [159], MYH9 [160], DOT1L [161], CXCL16 [162], PTEN (phosphatase and tensin homolog) [163], FOXO3 [164], DDIT4 [165], PINK1 [166], IQGAP1 [167], ADIPOR1 [168], MTMR3 [169], USF2 [170], SGK1 [171], GSTO2 [172], ETS2 [173], TKT (transketolase) [174], CMIP (c-Maf inducing protein) [175], THBD (granzyme A) [464], IFNG (interferon gamma) [465], IFIH1 [466], STAT1 [467], CCR5 [468], ADCY5 [469], MT2A [470], DPP4 [471], FASLG (Fas ligand)…”

Section: Discussionmentioning

confidence: 99%

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

Vastrad¹,

Vastrad²

2021

Preprint

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Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2)/ coronavirus disease 2019 (COVID-19) infection is the leading cause of respiratory tract infection associated mortality worldwide. The aim of the current investigation was to identify the differentially expressed genes (DEGs) and enriched pathways in COVID-19 infection and its associated complications by bioinformatics analysis, and to provide potential targets for diagnosis and treatment. Valid next-generation sequencing (NGS) data of 93 COVID 19 samples and 100 non COVID 19 samples (GSE156063) were obtained from the Gene Expression Omnibus database. Gene ontology (GO) and REACTOME pathway enrichment analysis was conducted to identify the biological role of DEGs. In addition, a protein-protein interaction network, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network and receiver operating characteristic curve (ROC) analysis were used to identify the key genes. A total of 738 DEGs were identified, including 415 up regulated genes and 323 down regulated genes. Most of the DEGs were significantly enriched in immune system process, cell communication, immune system and signaling by NTRK1 (TRKA). Through PPI, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network analysis, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were selected as hub genes, which were expressed in COVID-19 samples relative to those in non COVID-19 samples, respectively. Among them, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were suggested to be diagonstic factors for COVID-19. The findings from this bioinformatics analysis study identified molecular mechanisms and the key hub genes that might contribute to COVID-19 infection and its associated complications.

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Knockdown of circ-FANCA alleviates LPS-induced HK2 cell injury via targeting miR-93-5p/OXSR1 axis in septic acute kidney injury

Cited by 50 publications

References 40 publications

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

CircTLK1 modulates sepsis‐induced cardiomyocyte apoptosis via enhancing PARP1/HMGB1 axis–mediated mitochondrial DNA damage by sponging miR‐17‐5p

Suppression of lncRNA GAS6-AS2 alleviates sepsis-related acute kidney injury through regulating the miR-136-5p/OXSR1 axis in vitro and in vivo

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

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