KCNQ1OT1 affects the progression of diabetic retinopathy by regulating miR‐1470 and epidermal growth factor receptor

Shao, Jun; Yin, Xin; Fan, Guangming; Tan, Chengye; Yao, Yong; Xin, Yu; Sun, Chao

doi:10.1002/jcp.28344

Cited by 30 publications

(27 citation statements)

References 33 publications

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“…Recent studies have con rmed that KCNQ1OT1 plays a vital role in diabetic complications, such as diabetic cardiomyopathy[6], diabetic nephropathy[8], and diabetic ocular disease [9,17]. KCNQ1OT1 and NLRP3 in ammasome are triggered in the corneal endothelium of diabetic patients and mice, as well as in HG-treated corneal endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of KCNQ1OT1 is elevated in HG-treated human retinal endothelial cells (hRECs) and in the aqueous humor of patients with DR compared with the normal control group. KCNQ1OT1 promotes DR progression by the regulation of miR-1470 and epidermal growth factor receptor (EGFR) [17]. However, whether KCNQ1OT1 is involved in regulating NLRP3 in ammasome activation of Müller cells in DR remains unknown.…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of KCNQ1OT1 Alleviates the Activation of NLRP3 Inflammasome Through miR-17-5p/TXNIP Axis in Retinal Müller Cells

Liu¹,

Cao²,

Dong³

et al. 2021

Preprint

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Diabetic retinopathy (DR) is one of the most severe and common complications caused by diabetic mellites. Inhibiting NLRP3 inflammasome activation displays a crucial therapeutic value in DR. Studies have shown that KCNQ1OT1 plays a critical role in regulating NLRP3 inflammasome activation and participates in the pathogenesis of diabetic complications. The present study aims to explore the role, and the potential mechanism of KCNQ1OT1 in regulating the activation of NLRP3 inflammasome in DR. The expression of KCNQ1OT1 and the activation of NLRP3 inflammasome were increased in experimental DR models. KCNQ1OT1 knockdown alleviated NLRP3 inflammasome-associated molecules expression. In addition, KCNQ1OT1 was found to be localized mainly in the cytoplasm of Müller cells and facilitated TXNIP expression by acting as a miR-17-5p sponge. KCNQ1OT1 promoted the activation of NLRP3 inflammasome through miR-17-5p/TXNIP axis. Moreover, the clinical samples of patients with DR showed that the expression of KCNQ1OT1 and the activation of NLRP3 inflammasome were all increased, further supporting the hypothesis that the KCNQ1OT1 dysregulation may be the molecular mechanism of the pathogenesis of DR. Therefore, KCNQ1OT1 may serve as a new therapeutic target for DR.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Knockdown of KCNQ1OT1 Alleviates the Activation of NLRP3 Inflammasome Through miR-17-5p/TXNIP Axis in Retinal Müller Cells

Liu¹,

Cao²,

Dong³

et al. 2021

Preprint

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“…36 Additionally, it is reported that KCNQ1OT1 accelerates the development of diabetic retinopathy by targeting miR-1470. 37 We supposed that KCNQ1OT1 might also be a ceRNA, so we worked out XIAP is a modulator in cell viability, apoptosis, and inflammatory responses. For example, studies have demonstrated that CCN1 promoted FasL-induced apoptosis of H9c2 cardiomyocytes by disrupting XIAP.…”

Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 attenuates sepsis-induced myocardial injury via regulating miR-192-5p/XIAP axis

Sun

Yuan

et al. 2020

Exp Biol Med (Maywood)

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Myocardial dysfunction is a prime cause of death in sepsis. This study is to delve into the function of lncRNA KCNQ1OT1 in myocardial injury induced by sepsis. Sepsis-induced myocardial injury model in rat was initiated by intraperitoneally injecting of LPS (10 mg/kg) in vivo, and cardiomyocyte H9c2 was treated with LPS to mimic sepsis in vitro. KCNQ1OT1 and miR-192-5p expressions were detected by qRT-PCR. The cell viability was probed with CCK-8 experiment and the apoptosis of the cardiomyocytes was tested using flow cytometry analysis. Western blot was operated to determine apoptosis-related proteins expressions. ELISA was used to evaluate the levels of TNF-α, IL-6, and IL-1β. Bioinformatics analysis, RT-PCR, dual luciferase reporter assay, and RNA immunoprecipitation experiment were utilized to detect the interrelation of genes. Herein, we proved that KCNQ1OT1 was considerably down-regulated, whereas miR-192-5p was markedly increased in myocardial tissues of septic rats. KCNQ1OT1 interrelated with miR-192-5p, and negatively modulated its expression levels. Overexpression of KCNQ1OT1 or the transfection of miR-192-5p inhibitors greatly facilitated the viability and impeded the apoptosis of H9c2 cardiomyocytes. miR-192-5p paired with the 3ʹUTR of XIAP, and repressed its protein expression, and XIAP was modulated positively by KCNQ1OT1. In conclusion, our work indicates that down-regulation of KCNQ1OT1 advances cardiac injury through regulating miR-192-5p/XIAP axis during sepsis. Impact statement Sepsis-induced cardiomyopathy remains to be a major challenge to health care systems around the globe. There are no known therapies currently available that can cure the disease. This study provides convincing evidence that KCNQ1OT1 could attenuate sepsis-mediated myocardial injury. We further demonstrate that the beneficial function of KCNQ1OT1 was achieved by regulating the miR-192-5p/XIAP axis. We therefore found a new mechanism of cardioprotective effect of KCNQ1OT1, one which also offers a novel theoretical basis for the therapy of sepsis-induced cardiomyopathy.

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“…LncRNAs play significant roles in modulating mRNA stability, functioning as miRNA sponges that compete for endogenous RNAs. 25,26 To further explore whether specific miRNAs are sponged by KCNQ1OT1, we identified miRNAs that were differentially expressed between intact control bone and postfracture calluses in a mouse model of fracture healing. Based on searches of the GEO database, we selected miR-701-3p.…”

Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 accelerates fracture healing via modulating miR‐701‐3p/FGFR3 axis

et al. 2020

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Emerging evidence highlights the role of the long noncoding RNA (lncRNA) KCNQ1OT1 in fracture healing. Osteoblast proliferation, migration, and survival are pivotal during this process. In this study, we aimed to improve our understanding of the regulatory role of lncRNA KCNQ1OT1 during osteoblast proliferation, migration, and survival. We searched the gene expression omnibus databases and LncBase Experimental V.2 to identify key microRNAs (miRNAs) targets of KCNQ1OT1. MiR‐701‐3p was selected as a differentially expressed miRNA and RNA immunoprecipitation assays were performed to verify its interaction with KCNQ1OT1. Fibroblast growth factor receptor 3 (FGFR3) was also identified as a target of miR‐701‐3p. We further identified KCNQ1OT1 as a competing endogenous RNA of miR‐701‐3p that could influence osteoblast proliferation, migration, and apoptosis in vitro and in vivo. Taken together, our results indicate that the KCNQ1OT1/miR‐701‐3p/FGFR3 axis is an important regulator of osteoblast proliferation, migration, and apoptosis, and provide a new therapeutic avenue for fracture healing.

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KCNQ1OT1 affects the progression of diabetic retinopathy by regulating miR‐1470 and epidermal growth factor receptor

Cited by 30 publications

References 33 publications

Knockdown of KCNQ1OT1 Alleviates the Activation of NLRP3 Inflammasome Through miR-17-5p/TXNIP Axis in Retinal Müller Cells

Knockdown of KCNQ1OT1 Alleviates the Activation of NLRP3 Inflammasome Through miR-17-5p/TXNIP Axis in Retinal Müller Cells

LncRNA KCNQ1OT1 attenuates sepsis-induced myocardial injury via regulating miR-192-5p/XIAP axis

LncRNA KCNQ1OT1 accelerates fracture healing via modulating miR‐701‐3p/FGFR3 axis

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