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LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte

One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing. In response to injury, EMT is required to activate and mobilize statio...

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Autores principales: Zhang, Liping, Hu, Junyi, Meshkat, Bahar I., Liechty, Kenneth W., Xu, Junwang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8584148/
https://www.ncbi.nlm.nih.gov/pubmed/34769245
http://dx.doi.org/10.3390/ijms222111816
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author Zhang, Liping
Hu, Junyi
Meshkat, Bahar I.
Liechty, Kenneth W.
Xu, Junwang
author_facet Zhang, Liping
Hu, Junyi
Meshkat, Bahar I.
Liechty, Kenneth W.
Xu, Junwang
author_sort Zhang, Liping
collection PubMed
description One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing. In response to injury, EMT is required to activate and mobilize stationary keratinocytes in the skin toward the wound bed, which allows for re-epithelialization. This process is stalled in diabetic wounds. In this study, we investigate the role of long non-coding RNA (lncRNA), MALAT1, in transforming growth factor beta 1(TGF-β1)-induced EMT of human keratinocyte (HaCaT) cells. Initially, we detected MALAT1 and TGF-β1 expression in non-diabetic and diabetic wounds and found that these expression are significantly up-regulated in diabetic wounds. Then, HaCaT cells were cultured and exposed to TGF-β1. The EMT of HaCaT cells were confirmed by the increased expression of CDH2, KRT10, and ACTA2, in addition to the down-regulation of CDH1. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). MALAT1 silencing attenuates TGFβ1-induced EMT. Mechanistically, MALAT1 is involved in TGF-β1 mediated EMT through significantly induced ZEB1 expression, a critical transcription factor for EMT. In summary, lncRNA MALAT1 is involved in TGFβ1-induced EMT of human HaCaT cells and provides new understanding for the pathogenesis of diabetic wounds.
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spelling pubmed-85841482021-11-12 LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte Zhang, Liping Hu, Junyi Meshkat, Bahar I. Liechty, Kenneth W. Xu, Junwang Int J Mol Sci Article One of the major complications in diabetes is impaired wound healing. Unfortunately, effective therapies are currently lacking. Epithelial to mesenchymal transition (EMT) is a critical process involved in cutaneous wound healing. In response to injury, EMT is required to activate and mobilize stationary keratinocytes in the skin toward the wound bed, which allows for re-epithelialization. This process is stalled in diabetic wounds. In this study, we investigate the role of long non-coding RNA (lncRNA), MALAT1, in transforming growth factor beta 1(TGF-β1)-induced EMT of human keratinocyte (HaCaT) cells. Initially, we detected MALAT1 and TGF-β1 expression in non-diabetic and diabetic wounds and found that these expression are significantly up-regulated in diabetic wounds. Then, HaCaT cells were cultured and exposed to TGF-β1. The EMT of HaCaT cells were confirmed by the increased expression of CDH2, KRT10, and ACTA2, in addition to the down-regulation of CDH1. Knockdown of MALAT1 was achieved by transfecting a small interfering RNA (SiRNA). MALAT1 silencing attenuates TGFβ1-induced EMT. Mechanistically, MALAT1 is involved in TGF-β1 mediated EMT through significantly induced ZEB1 expression, a critical transcription factor for EMT. In summary, lncRNA MALAT1 is involved in TGFβ1-induced EMT of human HaCaT cells and provides new understanding for the pathogenesis of diabetic wounds. MDPI 2021-10-30 /pmc/articles/PMC8584148/ /pubmed/34769245 http://dx.doi.org/10.3390/ijms222111816 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhang, Liping
Hu, Junyi
Meshkat, Bahar I.
Liechty, Kenneth W.
Xu, Junwang
LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_full LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_fullStr LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_full_unstemmed LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_short LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_sort lncrna malat1 modulates tgf-β1-induced emt in keratinocyte
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8584148/
https://www.ncbi.nlm.nih.gov/pubmed/34769245
http://dx.doi.org/10.3390/ijms222111816
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