Non-coding RNA-Associated ceRNA Networks in a New Contrast-Induced Acute Kidney Injury Rat Model

Cheng, Wei; Li, Xuwei; Xiao, Yuzhong; Duan, Shao‐Bin

doi:10.1016/j.omtn.2019.05.011

Cited by 46 publications

(33 citation statements)

References 63 publications

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“…Iodinated CM-induced AKI accounts for 11% of cases of AKI and is the third most common cause of high morbidity and mortality in hospitalized patients [26]. Recent progress in interventional therapy and angiography has revived interest in explaining detailed mechanisms and developing effective treatment [27]. In our study, we investigated pyroptosis-related alterations that occur in renal tissues and renal tubule epithelial cells following IOP-induced AKI, suggesting that pyroptosis is a key event during CI-AKI.…”

Section: Discussionmentioning

confidence: 99%

Acetylbritannilactone attenuates contrast-induced acute kidney injury through its anti-pyroptosis effects

Chen

Yang

et al. 2020

Bioscience Reports

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Contrast-induced acute kidney injury (CI-AKI) is a severe complication caused by intravascular applied radial contrast media (CM). Pyroptosis is a lytic type of cell death inherently associated with inflammation response and the secretion of pro-inflammatory cytokines following caspase-1 activation. The aim of the present study was to investigate the protective effects of acetylbritannilactone (ABL) on iopromide (IOP)-induced acute renal failure and reveal the underlying mechanism. In vivo and in vitro, IOP treatment caused renal damage and elevated the caspase-1 (+) propidium iodide (PI) (+) cell count, interleukin (IL)-1β and IL-18 levels, lactate dehydrogenase (LDH) release, and the relative expression of nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3), apoptosis-associated speck-like protein (ASC), and gasdermin D (GSDMD), suggesting that IOP induces AKI via the activation of pyroptosis. Furthermore, the pretreatment of ABL partly mitigated the CI-AKI, development of pyroptosis, and subsequent kidney inflammation. These data revealed that ABL partially prevents renal dysfunction and reduces pyroptosis in CI-AKI, which may provide a therapeutic target for the treatment of CM-induced AKI.

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Section: Discussionmentioning

confidence: 99%

Acetylbritannilactone attenuates contrast-induced acute kidney injury through its anti-pyroptosis effects

Chen

Yang

et al. 2020

Bioscience Reports

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“…In recent years, an increasing number of lncRNAs and microRNAs have been associated with AKI [ 19 – 21 ]. For instance, the NEAT1 lncRNA induces hypoxia-triggered renal tubular epithelial cell apoptosis by sponging miR-27a-3p [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

LINC00052 ameliorates acute kidney injury by sponging miR-532-3p and activating the Wnt signaling pathway

Zheng

et al. 2020

Aging

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Acute kidney injury (AKI) is a complex renal disease. Long non-coding RNAs (lncRNAs) have frequently been associated with AKI. In the present study, we aimed to investigate the molecular mechanism(s) of LINC00052 in AKI. We found that LINC00052 expression was significantly decreased in AKI patient serum. In addition, in a hypoxic AKI cell model, LINC00052 expression was strongly elevated. In an I/R-triggered AKI rat model, the expression of TNF-α, IL-6 and IL-1β mRNA was strongly elevated. Moreover, we predicted miR-532-3p to be targeted by LINC00052 in AKI. Overexpression of LINC00052 increased hypoxia-induced inhibition of NRK-52E cell proliferation and reversed hypoxia-triggered apoptosis. Furthermore, we found that induction of TNF-α, IL-6 and IL-1β was repressed by overexpression of LINC00052. LINC00052 decreased hypoxia-induced ROS and MDA accumulation in vitro and increased SOD activity. Decreased levels of c-myc and cyclin D1 were observed in renal tissues of AKI rats. Lastly, Wnt/β-catenin signaling was inactivated in NRK-52E cells experiencing hypoxia, and LINC00052 upregulation reactivated Wnt/β-catenin signaling by sponging miR-532-3p. Taken together, these results suggest that LINC00052 ameliorates AKI by sponging miR-532-3p and activating Wnt signaling.

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“…For instance, XIST binds with miR-142-5p to upregulate PDCD4 and thus alleviates AKI 16 . The LINC00343/rno-miR-1956-5p/KCP axis is involved in contrast-induced AKI 17 . LINC00520 upregulates OSMR expression to promote AKI progression by binding with miR-27b-3p 18 .…”

Section: Introductionmentioning

confidence: 99%

c-MYC-induced long noncoding RNA MEG3 aggravates kidney ischemia–reperfusion injury through activating mitophagy by upregulation of RTKN to trigger the Wnt/β-catenin pathway

Liu

Zheng

et al. 2021

Cell Death Dis

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Ischemia–reperfusion injury (IRI)-induced acute kidney injury (AKI) is a life-threatening disease. The activation of mitophagy was previously identified to play an important role in IRI. Maternally expressed 3 (MEG3) can promote cerebral IRI and hepatic IRI. The present study was designed to study the role of MEG3 in renal IRI. Renal IRI mice models were established, and HK-2 cells were used to construct the in vitro models of IRI. Hematoxylin–eosin staining assay was applied to reveal IRI-triggered tubular injury. MitoTracker Green FM staining and an ALP kit were employed for detection of mitophagy. TdT-mediated dUTP-biotin nick-end labeling assay was used to reveal cell apoptosis. The results showed that renal cortex of IRI mice contained higher expression of MEG3 than that of sham mice. MEG3 expression was also elevated in HK-2 cells following IRI, suggesting that MEG3 might participate in the development of IRI. Moreover, downregulation of MEG3 inhibited the apoptosis of HK-2 cells after IRI. Mitophagy was activated by IRI, and the inhibition of MEG3 can restore mitophagy activity in IRI-treated HK-2 cells. Mechanistically, we found that MEG3 can bind with miR-145-5p in IRI-treated cells. In addition, rhotekin (RTKN) was verified to serve as a target of miR-145-5p. MEG3 upregulated RTKN expression by binding with miR-145-5p. Further, MEG3 activated the Wnt/β-catenin pathway by upregulation of RTKN. The downstream effector of Wnt/β-catenin pathway, c-MYC, served as the transcription factor to activate MEG3. In conclusion, the positive feedback loop of MEG3/miR-145-5p/RTKN/Wnt/β-catenin/c-MYC promotes renal IRI by activating mitophagy and inducing apoptosis, which might offer a new insight into the therapeutic methods for renal IRI in the future.

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Non-coding RNA-Associated ceRNA Networks in a New Contrast-Induced Acute Kidney Injury Rat Model

Cited by 46 publications

References 63 publications

Acetylbritannilactone attenuates contrast-induced acute kidney injury through its anti-pyroptosis effects

Acetylbritannilactone attenuates contrast-induced acute kidney injury through its anti-pyroptosis effects

LINC00052 ameliorates acute kidney injury by sponging miR-532-3p and activating the Wnt signaling pathway

c-MYC-induced long noncoding RNA MEG3 aggravates kidney ischemia–reperfusion injury through activating mitophagy by upregulation of RTKN to trigger the Wnt/β-catenin pathway

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