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

Zhao, Sheng; Wu, Chen; Li, Wei; Ye, Weimin; Li, Siqi; Rao, Ting; Ruan, Yuan; Zhou, Xiangjun; Liu, Cong; Qi, Yucheng

doi:10.1111/jcmm.16924

Cited by 10 publications

(7 citation statements)

References 51 publications

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“…In this study, we show that lncRNA-TUG1 is down-regulated in CKD, functions as miR-223-3p sponge by binding to its complementary site, and diminishes miR-223-3p-mediated Klotho suppression. Such sponge function of lncRNA-TUG1 is supported by earlier reports that several miRNAs including miR-145-5p 50 , miR-144-3p 53 , miR-29 58 can also bind to lncRNA-TUG1. The fact that lncRNA-TUG1 and miR-223-3p reciprocally antagonize each other underscores that they could form a double-negative feedback loop (Figure 8 k), which amplifies the capacity of miR-223-3p in suppressing Klotho expression.…”

Section: Discussionsupporting

confidence: 59%

“…Among them, lncRNA-TUG1 is known to be implicated in the pathogenesis of kidney diseases, although its function remains unclear and somewhat controversial. It has been reported that lncRNA-TUG1 exerts reno-protective effects by ameliorating fibrosis in diabetic nephropathy [49][50][51], attenuating ferroptosis [52] and apoptosis [53] of tubular epithelial cells in acute kidney injury, and enhancing mitochondrial function in podocytes [54]. However, lncRNA-TUG1 is also implicated in facilitating the development of CKD by inducing tubular epithelialmesenchymal transition [55,56], exacerbating inflammation and apoptosis of tubular cells [57].…”

Section: Discussionmentioning

confidence: 99%

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Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation

Zhang,

Li,

Tan

et al. 2024

Theranostics

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Background: Klotho deficiency is a common feature of premature aging and chronic kidney disease (CKD). As such, restoring Klotho expression could be a logic strategy for protecting against various nephropathies. In this study, we demonstrate that KP1, a Klotho-derived peptide, inhibits cellular senescence by restoring endogenous Klotho expression. Methods: The effects of KP1 on cellular senescence and Klotho expression were assessed in mouse models of CKD. RNA-sequencing was employed to identify the microRNA involved in regulating Klotho by KP1. Gain- or loss-of-function approaches were used to assess the role of miR-223-3p and IncRNA-TUG1 in regulating Klotho and cellular senescence. Results: KP1 inhibited senescence markers p21, p16 and γ-H2AX in tubular epithelial cells of diseased kidneys, which was associated with its restoration of Klotho expression at the posttranscriptional level. Profiling of kidney microRNAs by RNA sequencing identified miR-223-3p that bound to Klotho mRNA and inhibited its protein expression. Overexpression of miR-223-3p inhibited Klotho and induced p21, p16 and γ-H2AX, which were negated by KP1. Conversely, inhibition of miR-223-3p restored Klotho expression, inhibited cellular senescence. Furthermore, miR-223-3p interacted with lncRNA-TUG1 and inhibited its expression. Knockdown of lncRNA-TUG1 increased miR-223-3p, aggravated Klotho loss and worsened cellular senescence, whereas KP1 mitigated all these changes. Conclusion: These studies demonstrate that KP1 inhibits cellular senescence and induces Klotho expression via posttranscriptional regulation mediated by miR-223-3p and lncRNA-TUG1. By restoring endogenous Klotho, KP1 elicits a broad spectrum of protective actions and could serve as a promising therapeutic agent for fibrotic kidney disorders.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation

Zhang,

Li,

Tan

et al. 2024

Theranostics

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“…In addition, the jury through binding with miR-144-3p. 33) Meanwhile, Peg 13 was inactivated in cerebral I/R injury and its overexpression protected against I/R-induced brain injury. 20) In this study, our results indicated that Peg13 was downregulated in MIRI.…”

Section: Discussionmentioning

confidence: 99%

LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress

Wang,

Luo,

Yang

et al. 2024

Int. Heart J.

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Myocardial infarction/reperfusion (I/R) injury significantly impacts the health of older individuals. We confirmed that the level of lncRNA Peg13 was downregulated in I/R injury. However, the detailed function of Peg13 in myocardial I/R injury has not yet been explored.To detect the function of Peg13, in vivo model of I/R injury was constructed. RT-qPCR was employed to investigate RNA levels, and Western blotting was performed to assess levels of endoplasmic reticulum stress and apoptosis-associated proteins. EdU staining was confirmed to assess the cell proliferation.I/R therapy dramatically produced myocardial injury, increased the infarct area, and decreased the amount of Peg13 in myocardial tissues of mice. In addition, hypoxia/reoxygenation (H/R) notably induced the apoptosis and promoted the endoplasmic reticulum (ER) stress of HL-1 cells, while overexpression of Peg13 reversed these phenomena. Additionally, Peg13 may increase the level of Sirt1 through binding to miR-34a. Upregulation of Peg13 reversed H/R-induced ER stress via regulation of miR-34a/Sirt1 axis.LncRNA Peg13 reduces ER stress in myocardial infarction/reperfusion injury through mediation of miR-34a/Sirt1 axis. Hence, our research might shed new lights on developing new strategies for the treatment of myocardial I/R injury.

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“…Mechanistic experiments clarified that miR-144-3p could target and inhibit Nrf2 expression. Furthermore, lncRNA TUG1 could promote Nrf2 expression by sponging miR-144-3p and improving oxidative stress damage and apoptosis of cells and tissues [129]. In summary, the lncRNA TUG1/ miR-144-3p/Nrf2 axis provides a new therapeutic approach for renal IRI.…”

Section: Renal Irimentioning

confidence: 96%

Comprehensive overview of Nrf2-related epigenetic regulations involved in ischemia-reperfusion injury

et al. 2022

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Ischemic disease is a class of diseases in which an organ is ischemic due to vascular occlusion, a major contributor to death and disability worldwide. However, when the blood flow is restored, more severe damage occurs than ischemia alone and is known as ischemic-reperfusion injury (IRI). During reperfusion, the imbalance between the production of reactive oxygen species (ROS) and buffering capacity of the antioxidant defense system results in cell damage and death. Nuclear factor E2-related factor 2 (Nrf2) significantly affects antioxidant stress damage. The function of Nrf2 in the pathological process of IRI has been widely discussed, but the impact of epigenetic modifications associated with Nrf2 remains unclear. This article provides a comprehensive overview of the role and mechanism of Nrf2-related epigenetic modifications in the IRI of various organs, including the brain, heart, liver, and kidney. In addition, we summarize agonists that may target epigenetic regulation of Nrf2, which may be beneficial in seeking more effective strategies to improve IRI.

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

Cited by 10 publications

References 51 publications

Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation

Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation

LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress

Comprehensive overview of Nrf2-related epigenetic regulations involved in ischemia-reperfusion injury

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