LncRNA np_5318 promotes renal ischemia‑reperfusion injury through the TGF‑β/Smad signaling pathway

Lü, Jing; Miao, Jiangang; Sun, Jun

doi:10.3892/etm.2020.8534

Cited by 8 publications

(6 citation statements)

References 24 publications

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“…AKI refers to is a common complication in hospitalized patients and renal I/R injury is implicated in the pathophysiology of AKI [ 41 , 42 ]. As reported previously, numerous lncRNAs are upregulated in renal I/R injury [ 17 , 43 , 44 ]. For example, the expression of lncRNA MALAT1 in rats with renal I/R injury is distinctly higher than that in the control group [ 43 ].…”

Section: Discussionmentioning

confidence: 67%

“…For example, the expression of lncRNA MALAT1 in rats with renal I/R injury is distinctly higher than that in the control group [ 43 ]. The expression of lncRNA np_5318 is strikingly elevated in I/R-induced cell models of renal injury [ 44 ]. The expression of lncRNA TUG1 is markedly upregulated in renal tissues of I/R-induced rats compared with control group [ 17 ].…”

Section: Discussionmentioning

confidence: 99%

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Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion‐Induced Acute Kidney Injury by Regulating miR‐124‐3p/MMP2 Axis

Xue

Liu

Wang

et al. 2021

BioMed Research International

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Purpose. Ample evidence has proved that lncRNAs are pivotal regulators in acute kidney injury (AKI). Here, we focus on the role and mechanism of lncRNA SNHG14 in ischemia/reperfusion- (I/R-) caused AKI. Methods. I/R and hypoxia/reoxygenation (H/R) were applied to induce rats and HK-2 cells to establish AKI models in vivo and in vitro. Relative expression of SNHG14, miR-124-3p, and MMP2 was determined by qRT-PCR. HE staining was used to evaluate pathological changes in renal tissues, and acute tubular necrosis (ATN) score was calculated. Renal function was evaluated by measuring serum creatinine content and blood urea nitrogen content. Levels of IL-1β, IL-6, and TNF-α were measured by ELISA. Cell viability was examined by MTT assay. Oxidative stress was assessed by measuring SOD, MDA, and ROS levels. The target of SNHG14 or miR-124-3p was verified by DLR assay. Protein expression of MMP2 was examined by western blot. Results. SNHG14 was boosted in renal tissues of I/R-stimulated rats and H/R-induced HK-2 cells, while miR-124-3p was diminished in H/R-stimulated HK-2 cells. Si-SNHG14 or miR-124-3p mimics repressed inflammation and oxidative stress and enhanced cell viability in H/R-stimulated HK-2 cells. Sh-SNHG14 mitigated I/R-induced AKI in rats. MiR-124-3p was targeted by SNHG14, and MMP2 was targeted by miR-124-3p. Inhibition of miR-124-3p or upregulation of MMP2 reversed inhibitory effects of SNHG14 silence on inflammation and oxidative stress as well as the promoting effect of SNHG14 silence on cell viability in H/R-induced HK-2 cells. Conclusion. Knockdown of SNHG14 alleviated I/R-induced AKI by miR-124-3p-mediated downregulation of MMP2.

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Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion‐Induced Acute Kidney Injury by Regulating miR‐124‐3p/MMP2 Axis

Xue

Liu

Wang

et al. 2021

BioMed Research International

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“…Recently, numerous studies have indicated that long noncoding RNAs (lncRNAs) are tightly related to IRI, such as lncRNA MALAT1 in myocardial IRI [ 13 ], lncRNA AK139328 in hepatic IRI [ 14 ], and lncRNA np_5318 in RI/RI [ 15 ]. It has been well documented that lncRNA X-inactive-specific transcript (XIST) takes part in the regulation of many kidney diseases.…”

Section: Introductionmentioning

confidence: 99%

Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury

Chen

Xie

et al. 2020

Mediators of Inflammation

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Objective. Renal ischemia/reperfusion injury (RI/RI) is the main cause of acute kidney injury. Total glucosides of paeony (TGP) are a traditional Chinese medicine. This study was aimed at exploring the role of TGP in RI/RI and its underlying mechanism of action. Methods. Rat RI/RI models were constructed by surgical operation. Serum creatinine (Scr) and blood urea nitrogen (BUN) were used to evaluate renal function. The levels of proinflammatory cytokines were detected by ELISA. RI/RI was simulated by hypoxia/reoxygenation (H/R) treatment in renal cells in vitro. The lncRNA XIST (XIST) expression was analyzed by qRT-PCR. Then, the viability and apoptosis of renal cells were detected by MTT and flow cytometry assay. Additionally, dual-luciferase reporter assay was used to determine the interactions among XIST, microRNA-124-3p (miR-124-3p), and ITGB1. Results. TGP improved renal function and inhibited inflammatory responses after RI/RI. XIST expression was highly expressed in rat RI/RI models and H/R-treated renal cells, whereas treatment with TGP downregulated the XIST expression. Additionally, TGP increased viability and attenuated apoptosis and inflammation of H/R-treated renal cells via inhibiting XIST. Moreover, XIST was competitively bound to miR-124-3p, and ITGB1 was a target of miR-124-3p. miR-124-3p overexpression or ITGB1 inhibition rescued the reduction effect on viability and mitigated the promoting effects on cell apoptosis and inflammation caused by XIST overexpression in H/R-treated renal cells. Conclusions. In vivo, TGP attenuated renal dysfunction and inflammation in RI/RI rats. In vitro, TGP inhibited XIST expression to modulate the miR-124-3p/ITGB1 axis, alleviating the apoptosis and inflammation of H/R-treated renal cells.

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“…[40][41][42] Accumulating studies have revealed the important regulatory roles of lncRNAs in renal IRI including TUG1. [43][44][45] TUG1 was recently reported to play important roles in ischaemia-induced oxidative damage including in kidney, cardiac or cerebrum. 14,46,47 MiR-144-3p was confirmed to be a target of TUG1 in tumour models, 18,19 however, among all these studies related to oxidative damage, miR-144-3p was never studied as a target of TUG1.…”

Section: Discussionmentioning

confidence: 99%

LncRNA TUG1 attenuates ischaemia‐reperfusion‐induced apoptosis of renal tubular epithelial cells by sponging miR‐144‐3p via targeting Nrf2

Zhao

et al. 2021

J Cellular Molecular Medi

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Renal ischaemia-reperfusion injury (IRI), as a common type of clinical acute kidney injury (AKI), causes injury to the kidney and can even result in acute renal failure (ARF). 1,2 Convincing evidence has revealed the molecular and pathological events in AKI. [3][4][5] Oxidative stress plays a vital role in renal IRI-induced cell apoptosis and is the result of the imbalance between oxidative and antioxidant systems. 6,7 The production of excessive ROS eventually cause membrane lipid peroxidation and oxidative damage to proteins and DNA and lead to apoptosis and necrosis. 8MicroRNAs (miRNAs), small noncoding RNAs (ncRNAs), can regulate gene expression by targeting corresponding mRNAs. In

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LncRNA np_5318 promotes renal ischemia‑reperfusion injury through the TGF‑β/Smad signaling pathway

Cited by 8 publications

References 24 publications

Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion‐Induced Acute Kidney Injury by Regulating miR‐124‐3p/MMP2 Axis

Silence of Long Noncoding RNA SNHG14 Alleviates Ischemia/Reperfusion‐Induced Acute Kidney Injury by Regulating miR‐124‐3p/MMP2 Axis

Total Glucosides of Paeony Alleviate Cell Apoptosis and Inflammation by Targeting the Long Noncoding RNA XIST/MicroRNA-124-3p/ITGB1 Axis in Renal Ischemia/Reperfusion Injury

LncRNA TUG1 attenuates ischaemia‐reperfusion‐induced apoptosis of renal tubular epithelial cells by sponging miR‐144‐3p via targeting Nrf2

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