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Article: miR-200c Prevents TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Fibrogenesis in Mesothelial Cells by Targeting ZEB2 and Notch1
Title | miR-200c Prevents TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Fibrogenesis in Mesothelial Cells by Targeting ZEB2 and Notch1 |
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Authors | |
Keywords | Mesothelial cells miR-200c TGF-β1 EMT Fibrosis |
Issue Date | 2019 |
Publisher | Elsevier (Cell Press): OAJ. The Journal's web site is located at http://www.cell.com/molecular-therapy-family/nucleic-acids/latest-content |
Citation | Molecular Therapy - Nucleic Acids, 2019, v. 17, p. 78-91 How to Cite? |
Abstract | Peritoneal fibrosis and loss of transport function is a common complication contributing to adverse outcomes in patients on long-term peritoneal dialysis (PD). Epithelial-to-mesenchymal transition (EMT) in mesothelial cells is a salient feature, but its triggering mechanisms remain obscure. Dysregulation of microRNA (miR) expression is implicated in EMT and tissue fibrosis. We investigated the role of miR-200c in EMT and fibrogenesis in a murine PD model and in cultured peritoneal mesothelial cells. PD-fluid-treated mice showed peritoneal miR-200c expression reduced by 76.2% compared with PBS-treated mice, and this was accompanied by increased peritoneal α-smooth muscle actin, fibronectin, and collagen expression. PD fluid and TGF-β1 both reduced miR-200c expression in cultured mesothelial cells, accompanied by downregulation of E-cadherin and decorin, and induction of fibronectin, collagen I and III, and transcription factors related to EMT. Decorin prevented the suppression of miR-200c by TGF-β1. Lentivirus-mediated miR-200c overexpression prevented the induction of fibronectin, collagen I, and collagen III by TGF-β1, independent of decorin, and partially prevented E-cadherin suppression by TGF-β1. Target genes of miR-200c were identified as ZEB2 and Notch1. Our data demonstrate that miR-200c regulates EMT and fibrogenesis in mesothelial cells, and loss of peritoneal miR-200c contributes to PD-associated peritoneal fibrosis. |
Persistent Identifier | http://hdl.handle.net/10722/272563 |
ISSN | 2023 Impact Factor: 6.5 2023 SCImago Journal Rankings: 1.849 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Chu, JYS | - |
dc.contributor.author | Chau, MKM | - |
dc.contributor.author | Chan, CCY | - |
dc.contributor.author | Tai, ACP | - |
dc.contributor.author | Cheung, KF | - |
dc.contributor.author | Chan, TM | - |
dc.contributor.author | Yung, S | - |
dc.date.accessioned | 2019-07-23T04:08:04Z | - |
dc.date.available | 2019-07-23T04:08:04Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Molecular Therapy - Nucleic Acids, 2019, v. 17, p. 78-91 | - |
dc.identifier.issn | 2162-2531 | - |
dc.identifier.uri | http://hdl.handle.net/10722/272563 | - |
dc.description.abstract | Peritoneal fibrosis and loss of transport function is a common complication contributing to adverse outcomes in patients on long-term peritoneal dialysis (PD). Epithelial-to-mesenchymal transition (EMT) in mesothelial cells is a salient feature, but its triggering mechanisms remain obscure. Dysregulation of microRNA (miR) expression is implicated in EMT and tissue fibrosis. We investigated the role of miR-200c in EMT and fibrogenesis in a murine PD model and in cultured peritoneal mesothelial cells. PD-fluid-treated mice showed peritoneal miR-200c expression reduced by 76.2% compared with PBS-treated mice, and this was accompanied by increased peritoneal α-smooth muscle actin, fibronectin, and collagen expression. PD fluid and TGF-β1 both reduced miR-200c expression in cultured mesothelial cells, accompanied by downregulation of E-cadherin and decorin, and induction of fibronectin, collagen I and III, and transcription factors related to EMT. Decorin prevented the suppression of miR-200c by TGF-β1. Lentivirus-mediated miR-200c overexpression prevented the induction of fibronectin, collagen I, and collagen III by TGF-β1, independent of decorin, and partially prevented E-cadherin suppression by TGF-β1. Target genes of miR-200c were identified as ZEB2 and Notch1. Our data demonstrate that miR-200c regulates EMT and fibrogenesis in mesothelial cells, and loss of peritoneal miR-200c contributes to PD-associated peritoneal fibrosis. | - |
dc.language | eng | - |
dc.publisher | Elsevier (Cell Press): OAJ. The Journal's web site is located at http://www.cell.com/molecular-therapy-family/nucleic-acids/latest-content | - |
dc.relation.ispartof | Molecular Therapy - Nucleic Acids | - |
dc.rights | This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. | - |
dc.subject | Mesothelial cells | - |
dc.subject | miR-200c | - |
dc.subject | TGF-β1 | - |
dc.subject | EMT | - |
dc.subject | Fibrosis | - |
dc.title | miR-200c Prevents TGF-β1-Induced Epithelial-to-Mesenchymal Transition and Fibrogenesis in Mesothelial Cells by Targeting ZEB2 and Notch1 | - |
dc.type | Article | - |
dc.identifier.email | Chu, JYS: jyschu@hku.hk | - |
dc.identifier.email | Chan, CCY: calebccy@hku.hk | - |
dc.identifier.email | Tai, ACP: cpandrew@hku.hk | - |
dc.identifier.email | Chan, TM: dtmchan@hku.hk | - |
dc.identifier.email | Yung, S: ssyyung@hku.hk | - |
dc.identifier.authority | Chu, JYS=rp00684 | - |
dc.identifier.authority | Chan, TM=rp00394 | - |
dc.identifier.authority | Yung, S=rp00455 | - |
dc.description.nature | published_or_final_version | - |
dc.identifier.doi | 10.1016/j.omtn.2019.05.008 | - |
dc.identifier.pmid | 31226520 | - |
dc.identifier.pmcid | PMC6586597 | - |
dc.identifier.scopus | eid_2-s2.0-85067275129 | - |
dc.identifier.hkuros | 299783 | - |
dc.identifier.volume | 17 | - |
dc.identifier.spage | 78 | - |
dc.identifier.epage | 91 | - |
dc.identifier.isi | WOS:000487984400007 | - |
dc.publisher.place | United Kingdom | - |
dc.identifier.issnl | 2162-2531 | - |