Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1

Zhou, Xiangjun; Li, Yongwei; Wu, Cheng-Hung; Ye, Weimin

doi:10.1080/0886022x.2020.1818579

Cited by 10 publications

(7 citation statements)

References 35 publications

(35 reference statements)

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“…The salvage rate of the testis from a manual reduction to a surgical reduction ranges from 42 to 88% (Cattolica et al, 1982;Urkmez et al, 2018), so it is necessary to find an effective treatment for testicular torsion based on the molecular mechanism. The present research shows that lncRNAs play a crucial role in virous organs I/R progress (Lu et al, 2020;Zhou et al, 2020). Thus, it is crucial to elucidate the biological functions of lncRNAs in testicular I/R for better treatment of testicular torsion in the clinical practice.…”

Section: Discussionmentioning

confidence: 66%

Long Non-coding RNA MEG3 Promotes Pyroptosis in Testicular Ischemia-Reperfusion Injury by Targeting MiR-29a to Modulate PTEN Expression

Ning

et al. 2021

Front. Cell Dev. Biol.

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Increasing evidence shows that the abnormal long non-coding RNAs (lncRNAs) expression is closely related to ischemia-reperfusion injury (I/R) progression. Studies have previously described that lncRNA MEG3 regulates pyroptosis in various organs I/R. Nevertheless, the related mechanisms of MEG3 in testicular I/R has not been clarified. The aim of this research is to unravel underlying mechanisms of the regulation of pyroptosis mediated by MEG3 during testicular I/R. We have established a testicular torsion/detorsion (T/D) model and an oxygen-glucose deprivation/reperfusion (OGD/R)-treated spermatogenic cell model. Testicular ischemic injury was assessed by H&E staining. Western blotting, quantitative real-time PCR, MDA, and SOD tests and immunohistochemistry measured the expression of MEG3 and related proteins and the level of ROS production in testicular tissues. Quantitative real-time PCR and western blotting determined the relative expression of MEG3, miR-29a, and relevant proteins in GC-1. Cell viability and cytotoxicity were measured by CCK-8 and LDH assays. Secretion and expression levels of inflammatory proteins were determined by ELISA, immunofluorescence and western blotting. The interaction among MEG3, miR-29a, and PTEN was validated through a dual luciferase reporter assay and Ago2-RIP. In this research, we identified that MEG3 was upregulated in animal specimens and GC-1. In loss of function or gain of function assays, we verified that MEG3 could promote pyroptosis. Furthermore, we found that MEG3 negatively regulated miR-29a expression at the posttranscriptional level and promoted PTEN expression, and further promoted pyroptosis. Therefore, we explored the interaction among MEG3, miR-29a and PTEN and found that MEG3 directly targeted miR-29a, and miR-29a targeted PTEN. Overexpression of miR-29a effectively eliminated the upregulation of PTEN induced by MEG3, indicating that MEG3 regulates PTEN expression by targeting miR-29a. In summary, our research indicates that MEG3 contributes to pyroptosis by regulating miR-29a and PTEN during testicular I/R, indicating that MEG3 may be a potential therapeutic target in testicular torsion.

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Section: Discussionmentioning

confidence: 66%

Long Non-coding RNA MEG3 Promotes Pyroptosis in Testicular Ischemia-Reperfusion Injury by Targeting MiR-29a to Modulate PTEN Expression

Ning

et al. 2021

Front. Cell Dev. Biol.

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“…In addition, cyclin-dependent kinase inhibitor 2B antisense RNA1 (ANRIL) may prevent coronary atherosclerosis [27], and increased plasma levels of the lncRNAs H19 and LIPCAR are linked to increased risk of CAD [28]. Recent years, lncRNAs are gaining increasing recognition in chronic kidney disease and renal ischemia-reperfusion injury [29,30], not just in the cardiovascular state. lncRNA XLOC_032768 is beneficial to the anti-apoptosis ability of renal tubular epithelial cells and the regeneration and repair of kidney [29].…”

Section: Discussionmentioning

confidence: 99%

“…Recent years, lncRNAs are gaining increasing recognition in chronic kidney disease and renal ischemia-reperfusion injury [29,30], not just in the cardiovascular state. lncRNA XLOC_032768 is beneficial to the anti-apoptosis ability of renal tubular epithelial cells and the regeneration and repair of kidney [29]. lncRNAs may be relevant to osteogenic differentiation, presenting a new perspective into the mechanism of vascular calcification, which is a factor independently associated with cardiovascular death in patients with chronic kidney disease [30].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA PR11-387H17.6 as a potential novel diagnostic biomarker of atherosclerotic renal artery stenosis

Tian

Liu

et al. 2021

Renal Failure

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Background: Atherosclerotic renal artery stenosis (ARAS) is frequently related to ischemic nephropathy, secondary hypertension, and end-stage renal failure. Thus, this study aimed to explore whether certain circulating long noncoding RNAs (lncRNAs) may be used as potential specific ARAS biomarkers. Methods: In the present study, a microarray analysis was performed to screen for lncRNAs in renal artery tissue from four ARAS patients and four non-ARAS individuals. To identify specific lncRNAs as candidate potential biomarkers of ARAS, we used the following criteria: the fold change was set to >3.0 (compared with non-ARAS tissues), and p value cutoff was set at .05. According to these criteria, six lncRNAs were identified from 1150 lncRNAs. After validation by quantitative PCR (qPCR), these lncRNAs were independently validated in blood from groups of 18 ARAS patients, 18 non-ARAS individuals, and 18 healthy volunteers, furthermore, the predictive value of lncRNA PR11-387H17.6 was further assessed using blood from groups of 99 ARAS patients, 49 non-ARAS individuals, and 50 healthy volunteers. A receiver operating characteristic (ROC) curve analysis was performed to assess the performance of these lncRNAs as biomarkers. Results: In the ROC analysis, the area under the curve (AUC) of PR11-387H17.6 was 0.733, with 52.5% sensitivity and 84.8% specificity in predicting the occurrence of ARAS. After considering the risk factors, the AUC of PR11-387H17.6 was 0.844, and the optimal sensitivity increased from 52.5% to 74.5%, although the specificity decreased from 84.8% to 81.9%. In the multivariable logistic analysis, PR11-387H17.6 was an independent predictor of major adverse events (OR: 3.039; 95% CI: 1.388-6.654; p¼ .006). Conclusions: PR11-387H17.6 is a potential diagnostic biomarker of ARAS. The lncRNA levels in blood cells are regulated in ARAS. Thus, further investigations of the role of lncRNAs in ARAS are warranted.

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“…PRINS upregulates the expression of RANTES and directly causes significant renal inflammatory response. Recently, Zhou et al [77] identified lncRNA XLOC_032768 as a novel target in renal ischemia-reperfusion injury and its overexpression repressed the expression of fibronectin type III domain containing 3B and tubular epithelial cells apoptosis. Moreover, in the same mouse ischemia/reperfusion injury model, lncRNA Miat was upregulated and enhanced fibroblast formation, while lncRNA Rian was downregulated and also promoted fibroblast formation, both of which played different roles in the subsequent renal fibrosis of AKI, respectively.…”

Section: Noncoding Rnasmentioning

confidence: 99%

Epigenetic Modification Drives Acute Kidney Injury-to-Chronic Kidney Disease Progression

2021

Nephron

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Acute kidney injury (AKI) is a common clinical critical disease. Due to its high morbidity, increasing risk of complications, high mortality rate, and high medical costs, it has become a global concern for human health problems. Initially, researchers believed that kidneys have a strong ability to regenerate and repair, but studies over the past 20 years have found that kidneys damaged by AKI are often incomplete or even unable to repair. Even when serum creatinine returns to baseline levels, renal structural damage persists for a long time, leading to the development of chronic kidney disease (CKD). The mechanism of AKI-to-CKD transition has not been fully elucidated. As an important regulator of gene expression, epigenetic modifications, such as histone modification, DNA methylation, and noncoding RNAs, may play an important role in this process. Alterations in epigenetic modification are induced by hypoxia, thus promoting the expression of inflammatory factor-related genes and collagen secretion. This review elaborated the role of epigenetic modifications in AKI-to-CKD progression, the diagnostic value of epigenetic modifications biomarkers in AKI chronic outcome, and the potential role of targeting epigenetic modifications in the prevention and treatment of AKI to CKD, in order to provide ideas for the subsequent establishment of targeted therapeutic strategies to prevent the progression of renal tubular-interstitial fibrosis.

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Novel lncRNA XLOC_032768 protects against renal tubular epithelial cells apoptosis in renal ischemia–reperfusion injury by regulating FNDC3B/TGF-β1

Cited by 10 publications

References 35 publications

Long Non-coding RNA MEG3 Promotes Pyroptosis in Testicular Ischemia-Reperfusion Injury by Targeting MiR-29a to Modulate PTEN Expression

Long Non-coding RNA MEG3 Promotes Pyroptosis in Testicular Ischemia-Reperfusion Injury by Targeting MiR-29a to Modulate PTEN Expression

Long noncoding RNA PR11-387H17.6 as a potential novel diagnostic biomarker of atherosclerotic renal artery stenosis

Epigenetic Modification Drives Acute Kidney Injury-to-Chronic Kidney Disease Progression

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