Long noncoding RNA growth arrest‐specific transcript 5 alleviates renal fibrosis in diabetic nephropathy by downregulating matrix metalloproteinase 9 through recruitment of enhancer of zeste homolog 2

Zhang, Lei; Zhao, Shuai; Zhu, Yu Cheng

doi:10.1096/fj.201901380rr

Cited by 48 publications

(32 citation statements)

References 40 publications

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“…In lncRNA-GATA6-AS1, for example, FZD4 expression is reduced by recruiting EZH and H3K27me3 to the FZD4 promoter region [13]. Again, LncRNA GAS5 is known to downregulate MMP9 by recruiting EZH2 in the MMP9 promoter region [14]. Similarly, from our study, LINC01419 transcriptionally regulated target proliferation and migration-related genes by binding to EZH2.…”

Section: Agingsupporting

confidence: 66%

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

Zhang¹,

Chen

et al. 2020

Aging

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This study aims to investigate the biological role of LINC01419 and the underlying mechanism in HCC. RESULTS LINC01419 expression level is elevated in HCC tissues and is associated with a malignant phenotype In investigating the role of lncRNAs in HCC progression, the lncRNA expression profile was analyzed in HCC samples and non-HCC liver samples. The samples were obtained from TCGA datasets via circlncRNAnet (http://app.cgu.edu.tw/circlnc/) and TANRIC (http://ibl.mdanderson.org/tanric/_design/ basic/index.html). Several abnormal lncRNAs were detected and showed significant statistical differences. This study focused on LINC01419 because it showed the most significant difference (Figure 1A, Supplementary Figure 1A). The LINC01419 expression level was higher in HCC cell lines when compared to LO2 (normal liver cell line), (Figure 1B). To confirm whether

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Section: Agingsupporting

confidence: 66%

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

Zhang¹,

Chen

et al. 2020

Aging

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“…Increasing evidence have indicated lncRNAs' involvement in the pathogenesis of many diseases, including fibrosis [32][33][34]. Previous studies have showed that lncRNA PFAL contributed to the progression of pulmonary fibrosis [35].…”

Section: Agingmentioning

confidence: 99%

LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p

Wang

Zhang

et al. 2020

Aging

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Previous studies have shown that lncRNA small nuclear RNA host gene 7 (lncRNA SNHG7) played an important role in cancer progression. However, the role of lncRNA SNHG7 in cardiac fibrosis is still poorly understood. In this study, the results of quantitative real time polymerase chain reaction (qRT-PCR) analysis showed that lncRNA SNHG7 was over expressed in the infarcted and peri-infarcted area in the left ventricle after MI in mice. Western blot analysis showed that knockdown of SNHG7 decreased the expression of collagen type 1 (Col1)and α-smooth muscle actin (α-SMA). Echocardiographic study suggested that inhibition of SNHG7 improved cardiac function after MI in mice. Luciferase assay indicated SNHG7 could act as a competing endogenous RNA (ceRNA) by sponging miR-34-5p. The MTT cell proliferation assay and 5-ethynyl-2'-deoxyuridine (EdU) labelling assay revealed that co-transfection of SNHG7 and miR-34-5p inhibited cell viability and proliferation of cardiac fibroblasts (CF). All the results indicated that lncRNA SNHG7 could promote cardiac fibrosis via targeting miR-34-5p through acting as a ceRNA in mice after MI. Silencing of SNHG7 could attenuate deposition of collagens and improve cardiac function. miR-34-5p could suppress the fibrogenesis of CF by targeting ROCK1 and abolish SNHG7-induced CF proliferation and fibroblast-to-myofibroblast transition.

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“…Enhancer of zeste homolog 2 (EZH2) is a histone H3 lysine 27 (H3K27)-specific methyltransferase, and EZH2-mediated H3K27me3 is a suppressive posttranslational modification ( McCabe et al, 2012 ). Zhang, Zhao & Zhu (2020) demonstrated that GAS5 recruits EZH2 to the matrix metalloproteinase 9 (MMP9) promoter region, thereby resulting in a subsequent downregulation of MMP9 expression, which relieves renal fibrosis in diabetic nephropathy rats. EZH2-mediated H3K27 hypermethylation at the cyclooxygenase-2 (COX-2) promoter results in the epigenetic silencing of COX-2, facilitating the fibrotic process in idiopathic pulmonary fibrosis (IPF) ( Coward et al, 2014 ; Mozzetta et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

DZNep, an inhibitor of the histone methyltransferase EZH2, suppresses hepatic fibrosis through regulating miR-199a-5p/SOCS7 pathway

Ding

Zheng

et al. 2021

PeerJ

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Background Hepatic fibrosis is a common response to chronic liver injury. Recently, the role of DZNep (a histone methyltransferase EZH2 inhibitor) in repressing pulmonary and renal fibrosis was verified. However, the potential effect of DZNep on hepatic fibrosis has not been elucidated. Methods The hepatic fibrosis model was established in rats treated with CCl4 and in hepatic stellate cells (HSCs) treated with TGF-β1. The liver tissues were stained with H&E and Masson’s trichrome. The expression of EZH2, SOCS7, collagen I, αSMA mRNA and miR-199-5p was assessed using qPCR, immunohistochemical or western blot analysis. A dual-luciferase reporter assay was carried out to validate the regulatory relationship of miR-199a-5p with SOCS7. Results The EZH2 level was increased in CCl4-treated rats and in TGF-β1-treated HSCs, whereas DZNep treatment significantly inhibited EZH2 expression. DZNep repressed hepatic fibrosis in vivo and in vitro, as evidenced by the decrease of hepatic fibrosis markers (α-SMA and Collagen I). Moreover, miR-199a-5p expression was repressed by DZNep in TGF-β1-activated HSCs. Notably, downregulation of miR-199a-5p decreased TGF-β1-induced expression of fibrosis markers. SOCS7 was identified as a direct target of miR-199a-5p. The expression of SOCS7 was decreased in TGF-β1-activated HSCs, but DZNep treatment restore d SOCS7 expression. More importantly, SOCS7 knockdown decreased the effect of DZNep on collagen I and α SMA expression in TGF-β1-activated HSCs. Conclusions DZNep suppresses hepatic fibrosis through regulating miR-199a-5p/SOCS7 axis, suggesting that DZNep may represent a novel treatment for fibrosis.

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Long noncoding RNA growth arrest‐specific transcript 5 alleviates renal fibrosis in diabetic nephropathy by downregulating matrix metalloproteinase 9 through recruitment of enhancer of zeste homolog 2

Cited by 48 publications

References 40 publications

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

LINC01419 facilitates hepatocellular carcinoma growth and metastasis through targeting EZH2-regulated RECK

LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p

DZNep, an inhibitor of the histone methyltransferase EZH2, suppresses hepatic fibrosis through regulating miR-199a-5p/SOCS7 pathway

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