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:	Liping Zhang, Junyi Hu, Bahar I. Meshkat, Kenneth W. Liechty, Junwang Xu
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	diabetic wounds long non-coding RNA MALAT1 epithelial mesenchymal transition Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/48e0f2e340fe4c308854e13453d701d1
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spelling	oai:doaj.org-article:48e0f2e340fe4c308854e13453d701d12021-11-11T17:15:18ZLncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte10.3390/ijms2221118161422-00671661-6596https://doaj.org/article/48e0f2e340fe4c308854e13453d701d12021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11816https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067One 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.Liping ZhangJunyi HuBahar I. MeshkatKenneth W. LiechtyJunwang XuMDPI AGarticlediabetic woundslong non-coding RNAMALAT1epithelial mesenchymal transitionBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11816, p 11816 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	diabetic wounds long non-coding RNA MALAT1 epithelial mesenchymal transition Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	diabetic wounds long non-coding RNA MALAT1 epithelial mesenchymal transition Biology (General) QH301-705.5 Chemistry QD1-999 Liping Zhang Junyi Hu Bahar I. Meshkat Kenneth W. Liechty Junwang Xu LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
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.
format	article
author	Liping Zhang Junyi Hu Bahar I. Meshkat Kenneth W. Liechty Junwang Xu
author_facet	Liping Zhang Junyi Hu Bahar I. Meshkat Kenneth W. Liechty Junwang Xu
author_sort	Liping Zhang
title	LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte
title_short	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_sort	lncrna malat1 modulates tgf-β1-induced emt in keratinocyte
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/48e0f2e340fe4c308854e13453d701d1
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_version_	1718432114841485312

LncRNA MALAT1 Modulates TGF-β1-Induced EMT in Keratinocyte

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