LncRNA SOX2OT alleviates the high glucose-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis

Zhang, Yan; Chang, Baochao; Zhang, Jiqiang; Wu, Xueping

doi:10.1016/j.yexmp.2019.104283

Cited by 28 publications

(24 citation statements)

References 24 publications

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“…In our data, the abundance of miR-9-5p was increased in high glucose-induced podocytes, and miR-9-5p was validated to be the target miRNA for CASC2, and CASC2 could inversely modulate miR-9-5p expression in podocytes. Recovery experiments showed that CASC2 mitigated podocytes injury by decreasing miR-9-5p via acting as a miR-9-5p sponge, similar to the work of Zhang et al, who indicated that lncRNA SOX2OT could reduce the high glucose-stimulated podocytes damage by autophagy induction through binding to miR-9 [ 33 ]. Therefore, it is reasonable to infer that CASC2 regulated podocyte activity, apoptosis and autophagy through sponging miR-9-5p.…”

Section: Discussionsupporting

confidence: 67%

Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy

Dai

2020

Diabetol Metab Syndr

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Background High glucose (HG) induced podocytes injury plays an important role in diabetes nephropathy (DN) development. Long noncoding RNA cancer susceptibility candidate 2 (CASC2) was found to be decreased in serum of DN patients. We aimed to explore the function and possible mechanism of CASC2 in HG induced podocytes injury. Methods Under normal glucose (NG), HG and mannitol stimulated podocyte conditions, the levels of CASC2, microRNA-9-5p (miR-9-5p) and peroxisome proliferator-activated receptor gamma (PPARγ) were examined by quantitative real-time polymerase chain reaction (qRT-PCR). Podocyte injury was evaluated by measuring cell viability and apoptosis of CIHP-1 cells were checked by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Western blot was used to detect all protein levels. Dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the relationship between CASC2 and miR-9-5p. Results HG stimulation inhibited the expression levels of CASC2 and PPARγ, but promoted the expression of miR-9-5p. HG could restrain cell viability, autophagy and facilitate apoptosis in CIHP-1 cells, while CASC2 overexpression could reverse HG-induced podocytes injury. Furthermore, CASC2 could be used as a ceRNA to adsorb miR-9-5p, and miR-9-5p mimic overturned the effects of CASC2 on cell viability, autophagy and apoptosis in HG-stimulated podocytes. Additionally, PPARγ was a target gene of miR-9-5p, and CASC2 could weaken the HG-induced podocytes injury by up-regulating PPARγ. Conclusion CASC2 increased cell viability, autophagy and inhibited cell apoptosis by regulating miR-9-5p/PPARγ axis, thus reducing the HG-induced podocytes injury.

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Section: Discussionsupporting

confidence: 67%

Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy

Dai

2020

Diabetol Metab Syndr

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“…26 SOX2OT up-regulation attenuates the high glucoseinduced podocytes injury through autophagy via miR-9/ SIRT1 axis. 27 Our study first revealed that SOX2OT was highly expressed in heart tissues of HF mice and ISOinduced CFs, suggesting that SOX2OT was associated with HF. The changes of physiological indexes such as LVSP, LVEDP, and ±dp/dt max confirmed that SOX2OT silencing alleviated HF in mice.…”

Section: Discussionmentioning

confidence: 65%

LncRNA SOX2OT/Smad3 feedback loop promotes myocardial fibrosis in heart failure

Liao

et al. 2020

IUBMB Life

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Long noncoding RNA SOX2OT is associated with myocardial fibrosis (MF) in heart failure (HF). This article aims to investigate the role of SOX2OT in MF. We constructed HF mouse models by subcutaneous injection of isoprenaline (ISO). Cardiac fibroblasts (CFs) were treated with ISO to induce MF. Hematoxylin-eosin, Masson, and Sirius-red staining were used to identify myocardial injury and collagen deposition in heart tissues. The relationship among SOX2OT, miR-138-5p, TGF-β1, and Smad3 were evaluated by chromatin immunoprecipitation and luciferase reporter assay. The gene and protein expression were verified by quantitative real-time PCR and western blot. We found that SOX2OT was up-regulated in HF mice and ISO-induced CFs. SOX2OT knockdown reduced myocardial injury and collagen deposition in HF mice. The expression of collagen I, α-SMA, TGF-β1, and p-Smad3 were inhibited by SOX2OT down-regulation in HF mice and ISO-induced CFs. Furthermore, TGF-β1 was a target gene of miR-138-5p and indirectly regulated by SOX2OT. SOX2OT promoted MF in HF by activating TGF-β1/Smad3, and then Smad3 interacted with the SOX2OT promoter and formed a positive feedback loop. In conclusion, our work verifies that SOX2OT/Smad3 feedback loop promotes MF in HF. Thus, SOX2OT is potentially a novel therapeutic target for MF in HF.

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“…More importantly, lncRNA SOX2OT was confirmed to mitigate podocyte injury induced by the high glucose through autophagy induction by the miR-9/SIRT1 axis. Thus, SOX2OT may serve as a potential therapeutic target for DN [81]. It has been reported that lncRNA H2k2 could promote MC proliferation in DN via the miR-449a/b/Trim11/Mek signaling pathway [82].…”

Section: Lncrnas In Dnmentioning

confidence: 99%

Noncoding RNAs in Diabetic Nephropathy: Pathogenesis, Biomarkers, and Therapy

Mai

et al. 2020

Journal of Diabetes Research

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The correlation between diabetes and systematic well-being on human life has long established. As a common complication of diabetes, the prevalence of diabetic nephropathy (DN) has been increasing globally. DN is known to be a major cause of end-stage kidney disease (ESKD). Till now, the molecular mechanisms for DN have not been fully explored and the effective therapies are still lacking. Noncoding RNAs are a class of RNAs produced by genome transcription that cannot be translated into proteins. It has been documented that ncRNAs participate in the pathogenesis of DN by regulating inflammation, apoptosis, autophagy, cell proliferation, and other pathological processes. In this review, the pathological roles and diagnostic and therapeutic potential of three types of ncRNAs (microRNA, long noncoding RNA, and circular RNA) in the progression of DN are summarized and illustrated.

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LncRNA SOX2OT alleviates the high glucose-induced podocytes injury through autophagy induction by the miR-9/SIRT1 axis

Cited by 28 publications

References 24 publications

Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy

Long non-coding RNA cancer susceptibility candidate 2 (CASC2) alleviates the high glucose-induced injury of CIHP-1 cells via regulating miR-9-5p/PPARγ axis in diabetes nephropathy

LncRNA SOX2OT/Smad3 feedback loop promotes myocardial fibrosis in heart failure

Noncoding RNAs in Diabetic Nephropathy: Pathogenesis, Biomarkers, and Therapy

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