LncRNA SNHG16 induces proliferation and fibrogenesis via modulating miR-141-3p and CCND1 in diabetic nephropathy

Jiang, Xiaohong; Ru, Qianying; Li, Ping; Ge, Xin; Shao, Kan; Xi, Liuqing; Xu, Bojin; Wang, Qianqian; Huang, Shan

doi:10.1038/s41434-020-0160-x

Cited by 17 publications

(20 citation statements)

References 32 publications

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“…Nevertheless, some lncRNAs interact with miRNAs to trigger and promote the fibrotic process. (Yang et al, 2019a;Jiang et al, 2020a;Fu et al, 2020;Zhong et al, 2020). Interestingly, LINC00968 inhibits p21 by recruiting EZH2 to enhance proliferation and fibrosis of MCs (Li et al, 2018b).…”

Section: Non-smad-dependent Lncrnas In Dkdmentioning

confidence: 99%

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

Huang

et al. 2021

Front. Pharmacol.

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Diabetic kidney disease (DKD) is the most common diabetic complication and is a leading cause of end-stage kidney disease. Increasing evidence shows that DKD is regulated not only by many classical signaling pathways but also by epigenetic mechanisms involving chromatin histone modifications, DNA methylation, and non-coding RNA (ncRNAs). In this review, we focus on our current understanding of the role and mechanisms of ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) in the pathogenesis of DKD. Of them, the regulatory role of TGF-β/Smad3-dependent miRNAs and lncRNAs in DKD is highlighted. Importantly, miRNAs and lncRNAs as biomarkers and therapeutic targets for DKD are also described, and the perspective of ncRNAs as a novel therapeutic approach for combating diabetic nephropathy is also discussed.

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Section: Non-smad-dependent Lncrnas In Dkdmentioning

confidence: 99%

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

Huang

et al. 2021

Front. Pharmacol.

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“…The most up-to-date-version is available at https://doi.org/10.1042/BSR20204099 cancer [16], ovarian cancer [17] and prostate cancer [18]. More importantly, also as a member of SNHG family, SNHG16 has been confirmed to play a promoting role in the proliferation of HG-induced MMCs and fibrosis of DN tissues [19]. However, whether SNHG15 is involved in modulating inflammatory response and the development of DN remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Overexpression of miR-485 dampens the inflammation and proliferation of mesangial cells in an in vitro model of DN [22]. Of note, miR-141 has also been reported to act as a suppressor on DN in vitro [19,23]. Recent studies have revealed that the increased miR-141 expression significantly attenuates renal fibrosis [19,23] and cell proliferation [19].…”

Section: Introductionmentioning

confidence: 99%

“…Of note, miR-141 has also been reported to act as a suppressor on DN in vitro [19,23]. Recent studies have revealed that the increased miR-141 expression significantly attenuates renal fibrosis [19,23] and cell proliferation [19]. However, the effect of miR-141 on inflammation of MCs and the regulatory mechanism between miR-141 and SNHG15 have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

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SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axisin vitro

et al. 2021

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Long non-coding RNAs (lncRNAs) are confirmed to be involved in modulating diabetic nephropathy (DN). The present study is aimed to explore the regulatory mechanism of lncRNA small nucleolar RNA host gene 15 (SNHG15) on pediatric DN. Human glomerular mesangial cells (HGMCs) were exposed to high glucose (HG) to produce an in vitro model. The results showed that SNHG15 was remarkably up-regulated in pediatric DN tissues and HG-induced HGMCs. Functional experiments indicated that both silencing of SNHG15 and overexpression of miR-141 elevated the cell viability, and suppressed the inflammation in HG-induced HGMCs. SNHG15 was identified to be a lncRNA that could bind to miR-141, and ICAM-1 was a downstream target gene of miR-141. Both the low expression of miR-141 and high expression of ICAM-1 reversed the inhibiting effect of SNHG15 knockdown on inflammatory response, and the promoting effect on cell viability. To conclude, our study revealed that silencing of SNHG15 ameliorated the malignant behaviors of pediatric DN via modulating the miR-141/ICAM-1 axis in vitro.

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“…Our findings are the first demonstration of the contribution of NEAT1 to renal tubular injury during DN.It is well recognized that lncRNAs serve as a sponge of miRNAs to regulate downstream gene expression. For instance, lncRNA SNHG16 promoted the proliferation and fibrosis of mouse mesangial cells in HG conditions by modulating the miR-141-3p-CCND1 axis in DN(Jiang et al, 2020a) Liu et al (2020). showed that lncRNA MALAT1 promoted HG-induced pyroptosis by sequestering miR-30c to enhance NLRP3 expression during development of DN.…”

mentioning

confidence: 99%

LncRNA NEAT1 accelerates renal tubular epithelial cell damage by modulating mitophagy via miR‐150‐5p–DRP1 axis in diabetic nephropathy

Yang

Zhou

Liu

et al. 2021

Experimental Physiology

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Diabetic nephropathy (DN) is a severe complication in diabetic patients, with a high mortality rate. Renal tubular injury is involved in the pathogenesis of DN. In this study, we aimed to uncover the regulatory roles of the NEAT1-miR-150-5p-DRP1 axis in an in vitro model of DN and its possible mechanisms. High glucose-challenged HK-2 cells were used as an in vitro DN model. NEAT1, miR-150-5p and DRP1 levels were assessed by RT-qPCR. Cell viability was determined by the MTT assay. MitoSOX Red and JC-1 were used to evaluate intracellular production of reactive oxygen species and mitochondrial membrane potential, respectively. Lactate dehydrogenase release and superoxide dismutase activity were assessed with commercial kits. The protein levels of DRP1, p62, BECN1(beclin 1) and BNIP3 were determined by western blotting. The interaction between NEAT1 (DRP1) and miR-150-5p was verified by a dual-luciferase reporter assay and an RNA immunoprecipitation assay. Our results showed that in response to high glucose the NEAT1 and DRP1 levels were upregulated, whereas the miR-150-5p level was downregulated in HK-2 cells. Knockdown of NEAT1 or DRP1 in high glucose-challenged HK-2 cells inhibited excessive reactive oxygen species production and lactate dehydrogenase release, increased cell viability, mitochondrial membrane potential and superoxide dismutase activity and enhanced mitophagy. Inhibition of miR-150-5p resulted in the opposite results. Mechanistically, NEAT1 sponged miR-150-5p to increase the DRP1 level. Moreover, silencing of NEAT1 or DRP1 could counteract miR-150-5p inhibition-induced deleterious effects. Collectively, our findings indicate that NEAT1 facilitates high glucose-induced damage in HK-2 cells by suppressing mitophagy via the miR-150-5p-DRP 1 axis, which sheds light on a novel mechanism of DN.

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LncRNA SNHG16 induces proliferation and fibrogenesis via modulating miR-141-3p and CCND1 in diabetic nephropathy

Cited by 17 publications

References 32 publications

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease

SNHG15 knockdown inhibits diabetic nephropathy progression in pediatric patients by regulating the miR-141/ICAM-1 axisin vitro

LncRNA NEAT1 accelerates renal tubular epithelial cell damage by modulating mitophagy via miR‐150‐5p–DRP1 axis in diabetic nephropathy

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