The expression profiling and ontology analysis of noncoding RNAs in peritoneal fibrosis induced by peritoneal dialysis fluid

Li, Yanli; Guo, Runsheng; Hao, Guojun; Xiao, Jun; Yi, Bao; Zhou, Jing; Chen, Qinkai; Wei, Xin

doi:10.1016/j.gene.2015.03.050

Cited by 38 publications

(43 citation statements)

References 49 publications

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“…A previous study by Liu et al . (13) illustrated the wide range of IncRNAs, including AK089579, AK080622, and ENSMUST00000053838 as well as the JAK‐STAT, TGF‐β, and MAPK pathways, and their respective pivotal roles in PDF‐induced fibrotic peritoneum. Qu et al .…”

Section: Discussionmentioning

confidence: 99%

“…Liu et al . (13) implicated IncRNA AK089579 and the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway in the pathogenesis of PD fluid (PDF)‐induced PF. During the current study, the targeting relationship between microRNA‐296‐3p (miR‐296‐3p) and downstream of tyrosine kinase (DOK) 2 was determined through the application of an initial bioinformatics prediction followed by a confirmatory dual luciferase reporter assay.…”

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confidence: 99%

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Long noncoding RNA AK089579 inhibits epithelial‐to‐mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA‐296‐3p via DOK2 in peritoneal fibrosis

2019

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Peritoneal fibrosis (PF) represents a well‐recognized complication associated with continuous ambulatory peritoneal dialysis therapy, characterized by a reversible epithelial‐to‐mesenchymal transition (EMT) at the early stage. The aim of the current study was to investigate the effects linked with the long noncoding RNA (IncRNA) AK089579 on the EMT of peritoneal mesothelial cells (PMCs) as well as the associated regulatory mechanisms of AK089579 downstream of tyrosine kinase 2 (DOK2) and microRNA‐296‐3p (miR‐296‐3p). Enrichment analysis, gene intersection association analysis, and a gene‐gene intersection network were initially constructed to ascertain whether AK089579 regulated the expression of DOK2 through the mediation of miR‐296‐3p via the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in PF. After the PF mouse model had been constructed, the expression of the proteins associated with the JAK2/STAT3 signaling pathway and EMT and PMC migration and invasion were all determined accordingly. Based on the obtained results, AK089579 was determined to function as a competing endogenous RNA for miR‐296‐3p while acting to up‐regulate the expression of DOK2, which is a target gene of miR‐296‐3p. AK089579 was detected to confer an inhibitory effect on the activation of the JAK2/STAT3 signaling pathway, whereby the migration and invasion of PMCs among the mice models were suppressed. Meanwhile, up‐regulated miR‐296‐3p and down‐regulated DOK2 produced contrasting effects when compared with the aforementioned findings. Treatment with wpl0066, a JAK2/STAS3 signaling pathway inhibitor, was shown to reverse the effects exerted by up‐regulated miR‐296‐3p. Taken together, the central findings of the current study present evidence highlighting the capability of the IncRNA AK089579 to bind competitively to miR‐296‐3p and indirectly enhance the expression of DOK2, which in turn suppresses the activation of the JAK2/STAT3 signaling pathway, whereby the EMT, migration, and invasion of PMCs was inhibited in PF.—Zhang, X. W., Wang, L., Ding, H. Long noncoding RNA AK089579 inhibits epithelial‐to‐mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA‐296‐3p via DOK2 in peritoneal fibrosis. FASEB J. 33, 5112–5125 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Long noncoding RNA AK089579 inhibits epithelial‐to‐mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA‐296‐3p via DOK2 in peritoneal fibrosis

2019

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“…Chromatin modifications, especially histone acetylation, may also contribute to AKI sensitivity of CKD patients because inhibition of histone deacetylases showed beneficial effects in both CKD and AKI conditions 211–214 . As to the regulation of non-coding RNAs, genomic wide profiling has identified the dysregulation of multiple microRNAs in CKD, although the information about long non-coding RNAs is still limited 215–217 . The roles of specific microRNAs, such as mir-21, −192, and −29, have been delineated in CKD 218–223 , providing a foundation for further investigation of their involvement in AKI susceptibility of CKD patients.…”

Section: Potential Mechanisms Underlying the Susceptibility And mentioning

confidence: 99%

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

Wei

Liu

et al. 2017

Kidney International

311

222

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Acute kidney injury (AKI) and chronic kidney disease (CKD) are inter-connected. While AKI-to-CKD transition has been intensively studied, the information of AKI on CKD is very limited. Nonetheless, AKI, when occurring in CKD patients, is known to be more severe and difficult to recover. CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of TGF-β, p53, HIF, and major developmental pathways. At the cellular level, CKD is characterized by mitochondrial dysfunction, oxidative stress, and aberrant autophagy. At the tissue level, CKD is characterized by chronic inflammation and vascular dysfunction. These pathological changes may contribute to the heightened sensitivity of, and non-recovery from, AKI in CKD patients.

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“…Many genes and cytokines in HSCs are involved in the pathogenesis of liver fibrosis. Increasing modification manners in fibrosis processes were found at gene expressions including long noncoding RNAs (lncRNAs) (4). lncRNAs represent a group of transcripts that are .200 nt in length but without protein coding potential (5).…”

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confidence: 99%

linc‐SCRG1 accelerates liver fibrosis by decreasing RNA‐binding protein tristetraprolin

Luo

Liu

et al. 2018

FASEB j.

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The biologic roles of long noncoding RNAs (lncRNAs) in liver fibrosis remained unknown. Through microarray analysis, linc-SCRG1 (a lncRNA with transcript length 3118 bp) was found up-regulated 13.62-fold in human cirrhotic tissues. Quantitative PCR verified that linc-SCRG1 increased along with liver fibrosis progression in human tissues and in activated LX2 cells induced by TGF-β1. Knock-down of linc-SCRG1 significantly reversed the effects of TGF-β1 on LX2, including inhibiting activation, promoting apoptosis, reducing proliferation, lessening invasion, and down-regulating genes [fibrosis-related mRNA: α-smooth muscle actin ( α-SMA), type Ι collagen, and B-cell lymphoma-2; invasion-related mRNA: matrix metallopeptidase-2 ( MMP-2), MMP-9, and MMP-13; inflammation-related mRNA: TNF-α, IL-6, and IL-10]. linc-SCRG1 had binding sites with tristetraprolin (TTP), a kind of RNA-binding protein, and specifically combined to TTP proteins. Overexpression of linc-SCRG1 would cause TTP mRNA unstably and proteins decreasing. TTP mRNA was proved having negative relevance with linc-SCRG1 and was gradually reduced during human liver fibrosis progression. Overexpressing TTP resulted in knock-down of lincSCRG1 and degraded downstream target genes ( MMP-2 and TNF-α) in activated LX2. Overexpressing TTP had the same effects as small interfering RNA-lincSCRG1 (si- lincSCRG1), whereas knock-down of TTP had reversal effects on si- lincSCRG1 in activated LX2. In summary, linc-SCRG1 reduced TTP and restricted its degradation of target genes TNF-α and MMP-2. Therefore, linc-SCRG1 had a repressing TTP-elicited inactivation effect on hepatic stellate cell (HSC) phenotypes. Inhibition of linc-SCRG1 may be a novel therapeutic approach to inactivate HSCs and extenuate human liver fibrosis.-Wu, J.-C., Luo, S.-Z., Liu, T., Lu, L.-G., Xu, M.-Y. linc-SCRG1 accelerates liver fibrosis by decreasing RNA-binding protein tristetraprolin.

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The expression profiling and ontology analysis of noncoding RNAs in peritoneal fibrosis induced by peritoneal dialysis fluid

Cited by 38 publications

References 49 publications

Long noncoding RNA AK089579 inhibits epithelial‐to‐mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA‐296‐3p via DOK2 in peritoneal fibrosis

Long noncoding RNA AK089579 inhibits epithelial‐to‐mesenchymal transition of peritoneal mesothelial cells by competitively binding to microRNA‐296‐3p via DOK2 in peritoneal fibrosis

AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms

linc‐SCRG1 accelerates liver fibrosis by decreasing RNA‐binding protein tristetraprolin

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