A microrna screen to identify regulators of peritoneal fibrosis in a rat model of peritoneal dialysis

Lin, Fan; Wu, Xu; Zhang, Huidi; You, Xin; Zhang, Zhoucang; Shao, Rongrong; Huang, Chaoxing

doi:10.1186/s12882-015-0039-z

Cited by 20 publications

(22 citation statements)

References 57 publications

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“…Previous studies have presented evidence highlighting the key role played by RNAs in the formation of PD‐induced PF (19, 20). Liu et al .…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have presented evidence highlighting the key role played by RNAs in the formation of PD-induced PF (19,20). Liu et al (13), after sequencing the normal control peritoneum and PDF-induced fibrotic peritoneum, found 232 differentially expressed lncRNAs, among which AK089579 may play a key role in the formation of PF.…”

Section: Microarray-based Gene Expression Profiling Of Pfmentioning

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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“…Previous studies have presented evidence highlighting the key role played by RNAs in the formation of PD‐induced PF (19, 20). Liu et al .…”

Section: Resultsmentioning

confidence: 99%

Section: Microarray-based Gene Expression Profiling Of Pfmentioning

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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“…Among them, miRNA microarray technology is a specific and efficient method to generate miRNA expression profiles. This approach has been applied to study the functional linkages between miRNAs and physiological/pathological processes . In this study, a microarray that included 5214 mature human miRNAs on the array chip was employed to analyse miRNA expression systematically in the LPS‐treated PDLCs.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA expression profile of human periodontal ligament cells under the influence of Porphyromonas gingivalis LPS

Zhao

Wan

et al. 2016

J Cellular Molecular Medi

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Periodontitis is a chronic inflammatory disease which is caused by bacterial infection and leads to the destruction of periodontal tissues and resorption of alveolar bone. Thus, special attention should be paid to the mechanism under lipopolysaccharide (LPS)‐induced periodontitis because LPS is the major cause of periodontitis. However, to date, miRNA expression in the LPS‐induced periodontitis has not been well characterized. In this study, we investigated miRNA expression patterns in LPS‐treated periodontal ligament cells (PDLCs). Through miRNA array and differential analysis, 22 up‐regulated miRNAs and 28 down‐regulated miRNAs in LPS‐treated PDLCs were identified. Seven randomly selected up‐regulated (miR‐21‐5p, 498, 548a‐5p) and down‐regulated (miR‐495‐3p, 539‐5p, 34c‐3p and 7a‐2‐3p) miRNAs were examined by qRT‐PCR, and the results proved the accuracy of the miRNA array. Moreover, targets of these deregulated miRNAs were analysed using the miRWalk database. Database for Annotation, Visualization and Integration Discovery software were performed to analyse the Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway of differential expression miRNAs, and the results shown that Toll‐like receptor signalling pathway, cAMP signalling pathway, transforming growth factor‐beta signalling pathway, mitogen‐activated protein kinase (MAPK) signalling pathway and other pathways were involved in the molecular mechanisms underlying LPS‐induced periodontitis. In conclusion, this study provides clues for enhancing our understanding of the mechanisms and roles of miRNAs as key regulators of LPS‐induced periodontitis.

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“…However, to date, a limited number of studies investigated the role of miR-152 in the urinary system. In a recent study, Lin et al (31) demonstrated that miR-152 expression was significantly downregulated in a rat model of peritoneal fibrosis, suggesting its involvement in the pathogenesis of peritoneal fibrosis. Therefore, in the present study, it was hypothesized that miR-152 may serve similar roles in EMT of tubular epithelial cells and the progression of renal fibrosis.…”

Section: Discussionmentioning

confidence: 99%

miR‑152 regulates TGF‑β1‑induced epithelial‑mesenchymal transition by targeting HPIP in tubular epithelial cells

et al. 2018

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Renal fibrosis is a common pathological feature of chronic kidney diseases, and their development and progression are influenced by epigenetic modifications including aberrant microRNA (miRNA or miR) expression. miRNAs have been demonstrated to modulate the aggressiveness of various cancers and have emerged as possible therapeutic agents for the management of renal fibrosis. Transforming growth factor β1 (TGF‑β1)‑induced epithelial‑mesenchymal transition (EMT) of tubular epithelial cells serves a role in the initiation and progression of renal fibrosis. Furthermore, recent results indicated that the progression of EMT is reversible. The present study aimed to clarify the role of miR‑152 in EMT of the tubular epithelial cell line HK‑2, stimulated by TGF‑β1, using in vitro transfection with a miR‑152 mimic and to further investigate the underlying mechanism of miR‑152 activity. In the present study, miR‑152 expression was significantly reduced in TGF‑β1‑treated HK‑2 cells, accompanied by an increased expression of hematopoietic pre‑B‑cell leukemia transcription factor (PBX)‑interacting protein (HPIP). Additionally, miR‑152 overexpression inhibited TGF‑β1‑induced EMT and suppressed HPIP expression by directly targeting the 3' untranslated region of HPIP in HK‑2 cells. Furthermore, upregulation of HPIP reversed miR‑152‑mediated inhibitory effects on the EMT. Collectively, the results suggest that downregulation of miR‑152 initiates the dedifferentiation of renal tubules and progression of renal fibrosis, which may provide important targets for prevention strategies of renal fibrosis.

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A microrna screen to identify regulators of peritoneal fibrosis in a rat model of peritoneal dialysis

Cited by 20 publications

References 57 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

MicroRNA expression profile of human periodontal ligament cells under the influence of Porphyromonas gingivalis LPS

miR‑152 regulates TGF‑β1‑induced epithelial‑mesenchymal transition by targeting HPIP in tubular epithelial cells

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