LINC00162 participates in the pathogenesis of diabetic nephropathy via modulating the miR-383/HDAC9 signalling pathway

Fan, Wenxing; Wen, Xin; JinFeng, Zheng; Wang, KunHua; Qiu, Hui; Zhang, Jing; Su, Feng

doi:10.1080/21691401.2020.1773487

Cited by 12 publications

(4 citation statements)

References 24 publications

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“…The expression of NR_033515 in the kidney, peripheral blood, urine, and serum is increased compared with the control group [ 19 , 28 ], which is related to renal fibrosis, and enhance expression levels of fibrogenesis-related gene proteins (P38, ASK1, and ASK1), fibronectin and α -SMA [ 19 ]. lncRNA-NR_033515 promotes proliferation, fibrosis, and epithelial-mesenchymal transition in DKD.…”

Section: Discussionmentioning

confidence: 99%

The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses

Zhao

Yan

et al. 2022

Computational Intelligence and Neuroscience

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Background. Long noncoding RNA (lncRNA) is involved in the occurrence and development of diabetic kidney disease (DKD). It is necessary to identify the expression of lncRNA from DKD patients through systematic reviews, and then carry out silico analyses to recognize the dysregulated lncRNA and their associated pathways. Methods. The study searched Pubmed, Embase, Cochrane Library, WanFang, VIP, CNKI, and CBM to find lncRNA studies on DKD published before March 1, 2021. Systematic review of the literature on this topic was conducted to determine the expression of lncRNA in DKD and non-DKD controls. For the dysregulated lncRNA in DKD patients, silico analysis was performed, and lncRNA2Target v2.0 and starBase were used to search for potential target genes of lncRNA. The Encyclopedia of Genomics (KEGG) pathway enrichment analysis was performed to better identify dysregulated lncRNAs in DKD and determine the associated signal pathways. Results. According to the inclusion and exclusion criteria, 28 publications meeting the eligibility criteria were included in the systematic evaluation. A total of 3,394 patients were enrolled in this study, including 1,238 patients in DKD group, and 1,223 diabetic patients, and 933 healthy adults in control group. Compared with the control, there were eight lncRNA disorders in DKD patients (MALAT1, GAS5, MIAT, CASC2, NEAT1, NR_033515, ARAP1-AS2, and ARAP1-AS1). In addition, five lncRNAs (MALAT1, GAS5, MIAT, CASC2, and NEAT1) participated in disease-related signal pathways, indicating their role in DKD. Discussion. This study showed that there were eight lncRNAs in DKD that were persistently dysregulated, especially five lncRNAs which were closely related to the disease. Although systematic review included 28 studies that analyzed the expression of lncRNA in DKD-related tissues, the potential of these dysregulated lncRNAs as biomarkers or therapeutic targets for DKD remains to be further explored. Trial registration. PROSPERO (CRD42021248634).

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Section: Discussionmentioning

confidence: 99%

The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses

Zhao

Yan

et al. 2022

Computational Intelligence and Neuroscience

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“…58 LINC00162 promotes the progression of DN through the miR-383/HDAC9 signaling axis. 59 MiR-30a-5p improves the damage of immortalized rat podocytes. 60 In addition, studies have found that miR-485 was significantly reduced in DN patients’ serum, and it can also suppress the proliferation and inflammation of HMCs.…”

Section: Discussionmentioning

confidence: 97%

Quercetin attenuates the proliferation, inflammation, and oxidative stress of high glucose-induced human mesangial cells by regulating the miR-485-5p/YAP1 pathway

Wan

Wang

Pan

et al. 2022

Int J Immunopathol Pharmacol

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Background Diabetic nephropathy (DN) is a kidney damage caused by diabetes and the main cause of end-stage renal disease. However, the current treatment of DN has many limitations. Quercetin is a bioflavonoid compound with therapeutic benefits in metabolic diseases. This study aims to determine the therapeutic potentials and underlying mechanism of quercetin on DN. Methods We collected blood samples from DN patients and healthy controls and treated human mesangial cells (HMCs) with high glucose (HG) to establish an in vitro model of DN. Then we assessed the expression difference of miR-485-5p as well as YAP1 in serum of DN patients and healthy controls and between HG-induced HMCs and control cells. qRT-PCR and western blot were performed to assess miR-485-5p and YAP1 expression levels; CCK-8 and ELISAs were used to examine cell proliferation, inflammation, and oxidative stress. Dual luciferase reporter assay was implemented to detect the binding of miR-485-5p and YAP1 mRNA sequence. Results Quercetin suppressed proliferation, inflammation, and oxidative stress of HMCs induced by HG. As for mechanism, miR-485-5p directly bound to YAP1 and inhibited YAP1 expression. The downregulation of miR-485-5p and upregulation of YAP1 were also observed in the serum of DN patients. Quercetin modulated miR-485-5p/YAP1 axis to regulate HG-induced inflammation and oxidative stress. Conclusion: Quercetin inhibits the proliferation, inflammation, and oxidative stress of HMCs induced by HG through miR-485-5p/YAP1 axis, which might provide a novel treatment strategy for DN.

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“…Wang et al [48] showed that HDAC2/4/5 expression were upregulated in the kidneys of streptozotocininduced diabetic rats, diabetic db/db mice, and in kidney biopsies from diabetic patients (41). Another experiment showed that upregulation of HDAC9 was found to mediate podocyte injury and promote glomerulosclerosis in diabetic nephropathy mice (32), while analysis of GEO data also showed that HDAC9 expression was upregulated in renal tissue of diabetic nephropathy patients (42). Experimental rat and mice models of cerebral ischemia reperfusion (I/R) injury demonstrated that HDAC9 contributes to brain microvessel endothelial cell dysfunction (43,44).…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: HDAC9 promotes the susceptibility of diabetes to Contrast-induced acute kidney injury by regulating TXNIP/Trx1 pathway

Dai

Liu

et al. 2022

Preprint

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Background Contrast-induced acute kidney injury (CIAKI) is the third most common cause of hospital-acquired acute kidney injury. Diabetes mellitus (DM) is a major risk factor for CIAKI. Nevertheless, the mechanism of its role in diabetes susceptibility to CIAKI remains unclear. This study aimed to explore the role played by Histone deacetylase 9 (HDAC9) during the susceptibility of diabetic model to CIAKI. Methods Both in vitro and in vivo model of diabetes were induced by treating human renal tubular epithelial cells (HK-2) with high glucose (HG, 50mM) and by feeding mice with a high-fat diet (HFD) followed by intraperitoneal injection of streptozotocin (STZ), respectively. CIAKI mice models were constructed by contrast-media (iohexol), and iohexol also was treated HK-2 cells. Then, BRD-4354 (an inhibitor of HDAC9) was added into treated cells and mice. Finally, knockdown HDAC9 in HK-2 cultured with HG, and iohexol was added. The pathological changes, oxidative stress and apoptosis levels in mice kidney tissues were assessed. Meanwhile, cellular reactive oxygen species and the activity of HK-2 cells was measured. Western blot was used to determine the expression of HDAC9 and TXNIP/Trx1/P-ASK1/p38MAPK signaling pathways in cells and kidneys. Results HDAC9 was increased in both diabetic kidney tissues and HG-induced HK-2 cells. In vitro experiment indicated that HK-2 exposed to HG attenuated further damage to apoptosis and oxidative stress by iohexol via knockdown and inhibiting HDAC9. In vivo assay revealed that BRD-4354 reduced diabetic mice sensitivity to CI-AKI. Mechanically, HDAC9 could activate TXNIP/Trx1/P-ASK1/p38MAPK signaling pathway involving in the susceptibility of diabetes to CIAKI. Conclusion HDAC9 promotes the sensitivity of diabetes to CIAKI; and may be involved in oxidative stress and apoptosis through regulation of the TXNIP/Trx1/P-ASK1/p38MAPK pathway.

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LINC00162 participates in the pathogenesis of diabetic nephropathy via modulating the miR-383/HDAC9 signalling pathway

Abstract: View related articlesView Crossmark data Citing articles: 2 View citing articles LINC00162 participates in the pathogenesis of diabetic nephropathy via modulating the miR-383/HDAC9 signalling pathway

Cited by 12 publications

References 24 publications

The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses

The Impact of lncRNA on Diabetic Kidney Disease: Systematic Review and In Silico Analyses

Quercetin attenuates the proliferation, inflammation, and oxidative stress of high glucose-induced human mesangial cells by regulating the miR-485-5p/YAP1 pathway

WITHDRAWN: HDAC9 promotes the susceptibility of diabetes to Contrast-induced acute kidney injury by regulating TXNIP/Trx1 pathway

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