Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy

Li, Xue; Zeng, Li; Cao, Chuanwu; Lu, Chenhui; Lian, Weishuai; Han, Jianhong; Zhang, Xiaojun; Zhang, Jing; Tang, Tao; Li, Maoquan

doi:10.1016/j.yexcr.2016.12.006

Cited by 222 publications

(168 citation statements)

References 41 publications

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“…In diabetic nephropathy, knockdown of long intergenic noncoding RNA (lincRNA)‐Gm4419 inhibits inflammatory response and renal fibrosis by targeting NF‐κB/NLRP3 inflammasome signaling pathway (Yi et al, ). Additionally, MALAT1, a well‐studied lncRNA, directly repressed ELAVL1 and then decreased downstream NLRP3 expression via targeting miR‐23c, and thereby inhibited hyperglycemia‐triggered cell pyroptosis and inflammation (X. Li et al, ). MALAT1 could also suppress glucose‐induced upregulation of inflammatory mediators IL‐6 and TNF‐α through activation of SAA3 (Puthanveetil, Chen, Feng, Gautam, & Chakrabarti, ).…”

Section: Role Of Lncrnas In Akimentioning

confidence: 99%

Noncoding RNAs in acute kidney injury

Ren

Zhu

et al. 2018

Journal Cellular Physiology

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Acute kidney injury (AKI), caused by various stimuli including ischemia reperfusion, nephrotoxic insult, and sepsis, is characterized by abrupt decline of kidney function. Till now, the molecular mechanisms for AKI have not been fully explored and the effective therapies are still lacking. Noncoding RNAs (ncRNAs), a group of biomolecules function at RNA level, are involved in a wide range of physiopathological processes including AKI. MicroRNAs (miRNAs) are the most extensively studied ncRNAs in AKI. Evidence indicated that miRNAs are altered significantly in various types of AKI. Gain-and-loss-of-function studies demonstrated that miRNAs, such as miR-24, miR-126, miR-494, and miR-687, may bind to the 3'-untranslated region of their target genes to regulate inflammation, programmed cell death, and cell cycle in the injury and repair stages of AKI, indicating their therapeutic potential in AKI. In contrast, functions of long noncoding RNAs and circular RNAs in AKI are hot topics but still largely unknown. Additionally, ncRNAs packaged in exosome can be detected in circulation and urine, they may serve as specific biomarkers for AKI. This review summarized the alteration and functional role of ncRNAs and their therapeutic potential in AKI.

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Section: Role Of Lncrnas In Akimentioning

confidence: 99%

Noncoding RNAs in acute kidney injury

Ren

Zhu

et al. 2018

Journal Cellular Physiology

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“…The lncRNA taurine up-regulated 1 (TUG1) was reported to attenuate renal ECM deposition in DN mice via miRNA (miR)-377 and the target gene peroxisome proliferator activated receptor g (PPAR g) (9). The lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) can regulate cell apoptosis of renal tubular epithelial cells in DN rats via miR-23c and the target gene embryonic lethal, abnormal vision-like 1 (ELAVL1) (10). Our previous study also showed the lncRNA 1700020I14Rik mediates the hypoxia-inducible factor 1a signaling pathway through miR-34a-5p and the target gene Sirtuin 1, thereby improving fibrosis and proliferation of MCs in DN (11).…”

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confidence: 99%

The topological key lncRNA H2k2 from the ceRNA network promotes mesangial cell proliferation in diabetic nephropathyviathe miR‐449a/b/Trim11/Mek signaling pathway

et al. 2019

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Evidence has shown that long noncoding RNAs (IncRNAs) in the competing endogenous RNA (ceRNA) network are involved in various diseases. However, there is a lack of studies of the ceRNA network in diabetic nephropathy (DN). In this study, we investigated the effect of IncRNAs on mesangial cell (MC) proliferation in DN‐related ceRNA networks. Differences in IncRNA and mRNA expression between DN and normal mouse kidney tissues were detected with RNA‐seq, and DN‐related IncRNA/mRNA/microRNA (miRNA) ceRNA networks were constructed by R3.4.3. Computational analysis was performed, and expression and interactions between the topological RNAs were detected by bioinformatics methods, real‐time quantitative PCR (qPCR), and luciferase assay. Cell proliferation ability was measured by 5‐ethynyl‐2′‐deoxyuridine (EdU) in MCs cultured under high‐ or low‐glucose conditions. Moreover, the effect of the topological key IncRNA histocompatibility 2 K region locus 2 (H2k2) H2k2 on MC proliferation via the miRNA (miR)‐449a/b/triplet motif 11 (Trim11)/Mek signaling pathway was examined by EdU, flow cytometry analysis, and Western blot. In total, 153 IncRNAs, 428 mRNAs, and 2242 interactions were included in the constructed DN‐related ceRNA network. There were 15 RNAs in the top 5% of degree and betweenness. The expression of IncRNA H2k2 and mRNA Trim11 in MCs was increased in DN, which is consistent with the results of RNA‐seq and real‐time qPCR in vivo and in vitro. miR‐449a and miR‐449b, which were down‐regulated in MCs cultured with high glucose, were selected for further analysis. The results of real‐time qPCR and luciferase assay revealed the IncRNA H2k2‐miR‐449a/b‐Trim11 interaction in MCs. In addition, the data showed that H2k2 regulates MC proliferation via the miR‐449ab/Trim11/Mek signaling pathway. Taken together, these results provide new insight into the association between the topological key IncRNA H2k2 in the DN‐related ceRNA network and the miR‐449a/b/Trim11/Mek signaling pathway during MC proliferation in DN.—Chen, W., Peng, R., Sun, Y., Liu, H., Zhang, L., Peng, H., Zhang, Z. The topological key IncRNA H2k2 from the ceRNA network promotes mesangial cell proliferation in diabetic nephropathy via the miR‐449a/b/Trim11/Mek signaling pathway. FASEB J. 33, 11492–11506 (2019). http://www.fasebj.org

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“…Several reports have recently indicated the association between MALAT1 and renal tubular epithelial cells (HK‐2) injury . MALAT1 promotes HG‐induced HK‐2 cell pyroptosis, which plays an important role in the DN pathogenesis . MALAT1 also interacts with the transcription factor Foxo1 to represses SIRT1 transcription and promotes HG‐induced HK‐2 cell injury .…”

Section: Discussionmentioning

confidence: 99%

“…Of note, several recent reports have revealed the association between MALAT1 and DN . For example, Li et al observed increased MALAT1 expression in streptozotocin‐induced DN rats and in high glucose (HG)‐treated renal tubular epithelial cells (HK‐2). They also proposed that MALAT1 promotes pyroptosis in HK‐2 cells by functioning as a competitive endogenous RNA for miR‐23c to facilitate its target ELAVL1 .…”

Section: Introductionmentioning

confidence: 99%

“…For example, Li et al observed increased MALAT1 expression in streptozotocin‐induced DN rats and in high glucose (HG)‐treated renal tubular epithelial cells (HK‐2). They also proposed that MALAT1 promotes pyroptosis in HK‐2 cells by functioning as a competitive endogenous RNA for miR‐23c to facilitate its target ELAVL1 . However, these studies mainly focus on HK‐2; the role of MALAT1 in human renal glomerular endothelial cells (HRGECs) remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA MALAT1 mediates high glucose‐induced glomerular endothelial cell injury by epigenetically inhibiting klotho via methyltransferase G9a

Ren

2019

IUBMB Life

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Several recent reporters have indicated the potential role of long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in diabetic nephropathy (DN). However, these studies mainly focus on renal tubular epithelial cells HK‐2, the role of MALAT1 in human renal glomerular endothelial cells (HRGECs) remains unclear. Hence, this study aimed to explore the role of MALAT1 in high glucose (HG)‐induced HRGECs injury and the underlying epigenetic mechanism. Increased MALAT1 and decreased klotho expression were observed in both renal tissues from DN patients and HG‐exposed HRGECs. Furthermore, MALAT1 expression was negatively correlated with klotho expression. Moreover, both MALAT1 knockdown and klotho overexpression significantly abolished the HG‐induced HRGECs injury. Importantly, klotho overexpression reversed the MALAT1 overexpression‐mediated enhancement of the HG‐induced HRGECs injury. In addition, MALAT1 recruited G9a to elevate H3K9me1, which can bind to the klotho promoter and thus inhibited klotho transcription. In conclusion, MALAT recruits methyltransferase G9a to elevate H3K9me1 and epigenetically inhibits klotho expression, and thus mediates HG‐induced glomerular endothelial cell injury. © 2019 IUBMB Life, 1–9, 2019

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Long noncoding RNA MALAT1 regulates renal tubular epithelial pyroptosis by modulated miR-23c targeting of ELAVL1 in diabetic nephropathy

Cited by 222 publications

References 41 publications

Noncoding RNAs in acute kidney injury

Noncoding RNAs in acute kidney injury

The topological key lncRNA H2k2 from the ceRNA network promotes mesangial cell proliferation in diabetic nephropathyviathe miR‐449a/b/Trim11/Mek signaling pathway

Long noncoding RNA MALAT1 mediates high glucose‐induced glomerular endothelial cell injury by epigenetically inhibiting klotho via methyltransferase G9a

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