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Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway

While the skin is considered the first line of defense in the human body, there are some vulnerabilities that render it susceptible to certain threats, which is an issue that is recognized by both patients and doctors. Cutaneous wound healing is a series of complex processes that involve many types...

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Autores principales: Zhu, Junyao, Zhang, Mei, Gao, Yang, Qin, Xin, Zhang, Tianxu, Cui, Weitong, Mao, Chenchen, Xiao, Dexuan, Lin, Yunfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7366912/
https://www.ncbi.nlm.nih.gov/pubmed/32678073
http://dx.doi.org/10.1038/s41392-020-0173-3
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author Zhu, Junyao
Zhang, Mei
Gao, Yang
Qin, Xin
Zhang, Tianxu
Cui, Weitong
Mao, Chenchen
Xiao, Dexuan
Lin, Yunfeng
author_facet Zhu, Junyao
Zhang, Mei
Gao, Yang
Qin, Xin
Zhang, Tianxu
Cui, Weitong
Mao, Chenchen
Xiao, Dexuan
Lin, Yunfeng
author_sort Zhu, Junyao
collection PubMed
description While the skin is considered the first line of defense in the human body, there are some vulnerabilities that render it susceptible to certain threats, which is an issue that is recognized by both patients and doctors. Cutaneous wound healing is a series of complex processes that involve many types of cells, such as fibroblasts and keratinocytes. This study showed that tetrahedral framework nucleic acids (tFNAs), a type of self-assembled nucleic-acid material, have the ability to promote keratinocyte(HaCaT cell line) and fibroblast(HSF cell line) proliferation and migration in vitro. In addition, tFNAs increased the secretion of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in HSF cells and reduced the production of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) in HaCaT cells by activating the AKT-signaling pathway. During in vivo experiments, tFNA treatments accelerated the healing process in skin wounds and decreased the development of scars, compared with the control treatment that did not use tFNAs. This is the first study to demonstrate that nanophase materials with the biological features of nucleic acids accelerate the healing of cutaneous wounds and reduce scarring, which indicates the potential application of tFNAs in skin tissue regeneration.
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spelling pubmed-73669122020-07-21 Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway Zhu, Junyao Zhang, Mei Gao, Yang Qin, Xin Zhang, Tianxu Cui, Weitong Mao, Chenchen Xiao, Dexuan Lin, Yunfeng Signal Transduct Target Ther Article While the skin is considered the first line of defense in the human body, there are some vulnerabilities that render it susceptible to certain threats, which is an issue that is recognized by both patients and doctors. Cutaneous wound healing is a series of complex processes that involve many types of cells, such as fibroblasts and keratinocytes. This study showed that tetrahedral framework nucleic acids (tFNAs), a type of self-assembled nucleic-acid material, have the ability to promote keratinocyte(HaCaT cell line) and fibroblast(HSF cell line) proliferation and migration in vitro. In addition, tFNAs increased the secretion of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in HSF cells and reduced the production of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) in HaCaT cells by activating the AKT-signaling pathway. During in vivo experiments, tFNA treatments accelerated the healing process in skin wounds and decreased the development of scars, compared with the control treatment that did not use tFNAs. This is the first study to demonstrate that nanophase materials with the biological features of nucleic acids accelerate the healing of cutaneous wounds and reduce scarring, which indicates the potential application of tFNAs in skin tissue regeneration. Nature Publishing Group UK 2020-07-17 /pmc/articles/PMC7366912/ /pubmed/32678073 http://dx.doi.org/10.1038/s41392-020-0173-3 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Zhu, Junyao
Zhang, Mei
Gao, Yang
Qin, Xin
Zhang, Tianxu
Cui, Weitong
Mao, Chenchen
Xiao, Dexuan
Lin, Yunfeng
Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title_full Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title_fullStr Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title_full_unstemmed Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title_short Tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the AKT-signaling pathway
title_sort tetrahedral framework nucleic acids promote scarless healing of cutaneous wounds via the akt-signaling pathway
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7366912/
https://www.ncbi.nlm.nih.gov/pubmed/32678073
http://dx.doi.org/10.1038/s41392-020-0173-3
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