Fibroproliferative effect of microRNA-21 in hypertrophic scar derived fibroblasts
Copyright © 2016 Elsevier Inc. All rights reserved..
Hypertrophic scar (HS) is a fibroproliferative disorder caused by abnormal wound healing, which is characterized by excessive deposition of extracellular matrix (ECM) secreted by fibroblasts. We previous have found that expression of microRNA-21(miR-21) was increased in tissues and fibroblasts of HS. However, the underlying molecular mechanism remains to be further elucidated. In this study, we identified the miR-21 was a marker for the phenotype of HS fibroblasts, as anti-miR-21 reduced expression of fibrosis markers such as Col1A1, Col3A1, Fn and α-SMA in fibroblasts and overexpression of miR-21 promoted fibroproliferative expression in fibroblasts. Furthermore, we also found that miR-21 promoted TGF-β1 induced fibroproliferative expression by repressing Smad7 expression in vitro. In addition, the miR-21 inhibitor inhibited the growth of hypertrophic scar tissue in vivo (nude mice experimental model). These results indicated that miR-21 was a critical regulator for HS formation and TGF- β1/miR-21/Smad7 pathway could be a useful therapeutic target for the treatment of HS.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2016 |
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| Erschienen: |
2016 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:345 |
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| Enthalten in: |
Experimental cell research - 345(2016), 1 vom: 01. Juli, Seite 93-9 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Li, Guangzao [VerfasserIn] |
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| Links: |
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| Themen: |
Fibrosis |
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| Anmerkungen: |
Date Completed 15.05.2017 Date Revised 09.12.2017 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1016/j.yexcr.2016.05.013 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM260591025 |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2016 Elsevier Inc. All rights reserved. | ||
| 520 | |a Hypertrophic scar (HS) is a fibroproliferative disorder caused by abnormal wound healing, which is characterized by excessive deposition of extracellular matrix (ECM) secreted by fibroblasts. We previous have found that expression of microRNA-21(miR-21) was increased in tissues and fibroblasts of HS. However, the underlying molecular mechanism remains to be further elucidated. In this study, we identified the miR-21 was a marker for the phenotype of HS fibroblasts, as anti-miR-21 reduced expression of fibrosis markers such as Col1A1, Col3A1, Fn and α-SMA in fibroblasts and overexpression of miR-21 promoted fibroproliferative expression in fibroblasts. Furthermore, we also found that miR-21 promoted TGF-β1 induced fibroproliferative expression by repressing Smad7 expression in vitro. In addition, the miR-21 inhibitor inhibited the growth of hypertrophic scar tissue in vivo (nude mice experimental model). These results indicated that miR-21 was a critical regulator for HS formation and TGF- β1/miR-21/Smad7 pathway could be a useful therapeutic target for the treatment of HS | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Fibrosis | |
| 650 | 4 | |a Hypertrophic scar | |
| 650 | 4 | |a MiR-21 | |
| 650 | 4 | |a Smad7 | |
| 650 | 4 | |a TGF-β1 | |
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| 650 | 7 | |a Transforming Growth Factor beta1 |2 NLM | |
| 700 | 1 | |a Zhou, Renpeng |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Qi |e verfasserin |4 aut | |
| 700 | 1 | |a Jiang, Banghong |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Qingkai |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Chen |e verfasserin |4 aut | |
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