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Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus

The formation of wound epithelium initiates regeneration of amputated tail in Gekko japonicus. Energy metabolism is indispensable for the growth of living creatures and typically influenced by temperature. In this study, we reveal that low temperature lowers energy metabolism level and inhibits the...

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Autores principales: Wang, Qinghua, Mao, Zuming, Liu, Zhuang, Xu, Man, Huang, Shuai, Wang, Yin, Xu, Yanran, Qi, Longju, Liu, Mei, Liu, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515156/
https://www.ncbi.nlm.nih.gov/pubmed/36167813
http://dx.doi.org/10.1038/s42003-022-04004-5
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author Wang, Qinghua
Mao, Zuming
Liu, Zhuang
Xu, Man
Huang, Shuai
Wang, Yin
Xu, Yanran
Qi, Longju
Liu, Mei
Liu, Yan
author_facet Wang, Qinghua
Mao, Zuming
Liu, Zhuang
Xu, Man
Huang, Shuai
Wang, Yin
Xu, Yanran
Qi, Longju
Liu, Mei
Liu, Yan
author_sort Wang, Qinghua
collection PubMed
description The formation of wound epithelium initiates regeneration of amputated tail in Gekko japonicus. Energy metabolism is indispensable for the growth of living creatures and typically influenced by temperature. In this study, we reveal that low temperature lowers energy metabolism level and inhibits the regeneration of amputated tails of Gekko japonicus. We further find that low temperature attenuates the activation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) in regenerated tissues upon injury signals, and the inhibition of Akt hinders proliferation of the wound epithelium. Additionally, wingless/integrated (Wnt) inhibition suppresses epithelium proliferation and formation by inhibiting Akt activation. Finally, low temperature elevates the activity of adenylate-activated kinase (AMPK) pathway and in turn attenuates wound epithelium formation. Meanwhile, either mTOR downregulation or AMPK upregulation is associated with worse wound epithelium formation. Summarily, low temperature restricts wound epithelium formation by influencing energy sensory pathways including Akt/mTOR and AMPK signaling, which is also modulated by injury induced Wnt signal. Our results provide a mechanism that incorporates the injury signals with metabolic pathway to facilitate regeneration.
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spelling pubmed-95151562022-09-29 Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus Wang, Qinghua Mao, Zuming Liu, Zhuang Xu, Man Huang, Shuai Wang, Yin Xu, Yanran Qi, Longju Liu, Mei Liu, Yan Commun Biol Article The formation of wound epithelium initiates regeneration of amputated tail in Gekko japonicus. Energy metabolism is indispensable for the growth of living creatures and typically influenced by temperature. In this study, we reveal that low temperature lowers energy metabolism level and inhibits the regeneration of amputated tails of Gekko japonicus. We further find that low temperature attenuates the activation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) in regenerated tissues upon injury signals, and the inhibition of Akt hinders proliferation of the wound epithelium. Additionally, wingless/integrated (Wnt) inhibition suppresses epithelium proliferation and formation by inhibiting Akt activation. Finally, low temperature elevates the activity of adenylate-activated kinase (AMPK) pathway and in turn attenuates wound epithelium formation. Meanwhile, either mTOR downregulation or AMPK upregulation is associated with worse wound epithelium formation. Summarily, low temperature restricts wound epithelium formation by influencing energy sensory pathways including Akt/mTOR and AMPK signaling, which is also modulated by injury induced Wnt signal. Our results provide a mechanism that incorporates the injury signals with metabolic pathway to facilitate regeneration. Nature Publishing Group UK 2022-09-27 /pmc/articles/PMC9515156/ /pubmed/36167813 http://dx.doi.org/10.1038/s42003-022-04004-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/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/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wang, Qinghua
Mao, Zuming
Liu, Zhuang
Xu, Man
Huang, Shuai
Wang, Yin
Xu, Yanran
Qi, Longju
Liu, Mei
Liu, Yan
Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title_full Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title_fullStr Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title_full_unstemmed Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title_short Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus
title_sort akt/mtor integrate energy metabolism with wnt signal to influence wound epithelium growth in gekko japonicus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9515156/
https://www.ncbi.nlm.nih.gov/pubmed/36167813
http://dx.doi.org/10.1038/s42003-022-04004-5
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