A systematic integrative approach reveals novel microRNAs in diabetic nephropathy

Kiyanpour, Farnoush; Abedi, Maryam; Gheisari, Yousof

doi:10.4103/jrms.jrms_289_19

Cited by 11 publications

(6 citation statements)

References 51 publications

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“…After principal pivot analysis, 17 main regulatory ncRNAs were obtained, all of which were miRNAs, and 11 main regulatory TFs were obtained ( Fig 9 ). Analyzing the functions of miRNA and TF in previous studies, it was found that the non-coding genes hsa-miR-572 [ 21 ], hsa-miR-29a-3p [ 22 ], hsa-miR-29b-3p [ 23 ], hsa -miR-208a-3p [ 24 ], hsa-miR-153-3p [ 25 ], hsa-miR-29c-3p [ 26 ] may be related to diabetic nephropathy and transcription factors HIF1α [ 27 ], KLF4 [ 28 ], KLF5 [ 29 ], RUNX1 [ 30 ], SP1 [ 31 ], VDR [ 32 ], WT1 [ 33 ] may be related to diabetic nephropathy.…”

Section: Resultsmentioning

confidence: 99%

Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches

Liu

et al. 2021

PLoS ONE

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Diabetic nephropathy is one of the common microvascular complications of diabetes. Iron death is a recently reported way of cell death. To explore the effects of iron death on diabetic nephropathy, iron death score of diabetic nephropathy was analyzed based on the network and pathway levels. Furthermore, markers related to iron death were screened. Using RNA-seq data of diabetic nephropathy, samples were clustered uniformly and the disease was classified. Differentially expressed gene analysis was conducted on the typed disease samples, and the WGCNA algorithm was used to obtain key modules. String database was used to perform protein interaction analysis on key module genes for the selection of Hub genes. Moreover, principal component analysis method was applied to get transcription factors and non-coding genes, which interact with the Hub gene. All samples can be divided into two categories and principal component analysis shows that the two categories are significantly different. Hub genes (FPR3, C3AR1, CD14, ITGB2, RAC2 and ITGAM) related to iron death in diabetic nephropathy were obtained through gene expression differential analysis between different subtypes. Non-coding genes that interact with Hub genes, including hsa-miR-572, hsa-miR-29a-3p, hsa-miR-29b-3p, hsa-miR-208a-3p, hsa-miR-153-3p and hsa-miR-29c-3p, may be related to diabetic nephropathy. Transcription factors HIF1α, KLF4, KLF5, RUNX1, SP1, VDR and WT1 may be related to diabetic nephropathy. The above factors and Hub genes are collectively involved in the occurrence and development of diabetic nephropathy, which can be further studied in the future. Moreover, these factors and genes may be potential target for therapeutic drugs.

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Section: Resultsmentioning

confidence: 99%

Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches

Liu

et al. 2021

PLoS ONE

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“…Growing studies have demonstrated the essential role of TFs and miRNAs in the development of diabetes and its related complications. 56 , 57 In our study, a TFs‐miRNAs–mRNAs regulatory network was constructed which contained six miRNAs (has‐miR‐373‐3p, has‐miR‐493‐3p, has‐miR‐372‐3p, has‐miR‐152‐3p, has‐miR‐1‐3p, and has‐miR‐29a‐3p) and 1 TFs (Kruppel‐like factor 13 [KLF13]). KLF13 is an essential player in cell proliferation and differentiation, and has a critical role in the virus life cycle.…”

Section: Discussionmentioning

confidence: 99%

Exploration of the common pathogenic link between COVID‐19 and diabetic foot ulcers: An in silico approach

Cai,

Yang,

Shi

et al. 2023

Health Science Reports

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Background and AimsThe Coronavirus Disease‐19 (COVID‐19) is posing an ongoing threat to human health. Patients of diabetic foot ulcer (DFU) are susceptible to COVID‐19‐induced adverse outcomes. Nevertheless, investigations into their mutual molecular mechanisms have been limited to date. In the present work, we tried to uncover the shared pathogenesis and regulatory gene targets of COVID‐19 and DFU.MethodsIn this study, we chose GSE161281 as the COVID‐19 data set, which contained severe acute respiratory syndrome coronavirus 2 infected human induced embryonic stem cell‐derived peripheral neurons (n = 2) with uninfected controls (n = 2). The GSE134431 designated as the DFU data set, comprising full‐thickness DFU (n = 13) and diabetic foot skin (n = 8) samples from diabetic patients. The differential expressed genes (DEGs) were identified from GSE161281 and GSE134431, and the common DEGs between COVID‐19 and DFU were extracted. Multifactor regulatory network and co‐expression network of the common DEGs were analyzed, along with candidate drug prediction.ResultsAltogether, six common DEGs (dickkopf‐related protein 1 [DKK1], serine proteinase inhibitor A3 [SERPINA3], ras homolog family member D [RHOD], myelin protein zero like 3 [MPZL3], Claudin‐11 [CLDN11], and epidermal growth factor receptor pathway substrate 8‐like 1 [EPS8L1]) were found between COVID‐19 and DFU. Functional analyses indicated that pathways of apoptotic and Wnt signaling may contribute to progression of COVID‐19. Gene co‐expression network implied the shared pathways of immune regulation and cytokine response participated collectively in the development of DFU and COVID‐19. A multifactor regulatory network was constructed integrating the corresponding microRNAs (miRNAs) and transcription factors. Additionally, we proposed potential drug objects for the combined therapy.ConclusionOur study revealed the shared molecular mechanisms underlying COVID‐19 and DFU. The identified pivotal targets and common pathways can provide new perspectives for further research and assist the development of management strategies in patients of DFU complicated with COVID‐19.

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“…miR-208a-3p has been found to be involved in many diseases, including bone loss (26), cancer (27), and cardiovascular disease (28). Specially, miR-208a-3p was found to be highly expressed in the kidney of diabetic nephropathy patients and mouse model, and it may be involved in oxygen metabolism and regulation of cellular energy balance in diabetic nephropathy (29). Moreover, Zhu et al (30) found that miR-208a-3p expression was notably reduced in the myocardial tissue of acute myocardial infarction rats and miR-208a-3p overexpression in the myocardial tissue alleviated myocardial I/R injury.…”

Section: Introductionmentioning

confidence: 99%

miR-208a-3p regulated by circUQCRC2 suppresses ischemia/reperfusion-induced acute kidney injury by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis

Huang,

Meng,

Pang

et al. 2024

Shock

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Background Acute kidney injury (AKI) is a prevalent clinical syndrome with persistent kidney dysfunction. Renal ischemia/reperfusion (I/R) injury is a major cause of AKI. miR-208a-3p overexpression attenuated myocardial I/R injury. This study aims to investigate the role and mechanism of miR-208a-3p in I/R-induced AKI. Methods AKI models were established using hypoxia/reoxygenation (H/R)-exposed tubule epithelial cell HK-2 and I/R-induced mice. The function and mechanism of miR-208a-3p were investigated by gain-or loss-of-function methods using real-time PCR, CCK-8, flow cytometry, ELISA, western blot, hematoxylin-eosin staining, Tunel assay, detection of Fe2+, ROS, BUN and Creatinine, and luciferase reporter assay. Results miR-208a-3p expression was suppressed, while the expression of CELF2 and circular RNA ubiquinol-cytochrome c reductase core protein 2 (circUQCRC2) was increased in both AKI models. miR-208a-3p upregulation or circUQCRC2 silencing increased the viability, decreased the levels of proinflammatory cytokines (TNF-α, IL-1β and IL-6), reduced apoptosis and contents of Fe2+ and ROS, elevated expression of GPX4 and SLC7A11, reduced ACSL4 expression in H/R-stimulated HK-2 cells. Also, miR-208a-3p improved kidney function by alleviating renal injury, apoptosis, inflammation and ferroptosis in AKI mouse model. CELF2 was a target gene of miR-208a-3p which was negatively modulated by circUQCRC2. Overexpression of CELF2 blocked the function of miR-208a-3p upregulation or circUQCRC2 silencing on H/R-treated HK-2 cells. Moreover, the effects of circUQCRC2 downregulation on H/R-injured cells were also reversed by miR-208a-3p inhibitor. Conclusions miR-208a-3p regulated by circUQCRC2 could attenuate I/R-induced AKI by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis. This study provides potential therapeutic targets for I/R-induced AKI.

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A systematic integrative approach reveals novel microRNAs in diabetic nephropathy

Cited by 11 publications

References 51 publications

Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches

Bioinformatics analysis of genes related to iron death in diabetic nephropathy through network and pathway levels based approaches

Exploration of the common pathogenic link between COVID‐19 and diabetic foot ulcers: An in silico approach

miR-208a-3p regulated by circUQCRC2 suppresses ischemia/reperfusion-induced acute kidney injury by inhibiting CELF2-mediated tubular epithelial cell apoptosis, inflammation and ferroptosis

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