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Oxytocin promotes hepatic regeneration in elderly mice
Liver aging impairs the ability of hepatocyte regeneration. Recent studies have found that oxytocin (OT) plays an important role in promoting tissue repair and maintaining differentiation and regeneration of stem cells. Here, we reported that OT receptors, which are specifically located in hepatocyt...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7895748/ https://www.ncbi.nlm.nih.gov/pubmed/33659883 http://dx.doi.org/10.1016/j.isci.2021.102125 |
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author | Luo, Dan Jin, Bin Zhai, Xiangyu Li, Jing Liu, Chuanyong Guo, Wei Li, Jingxin |
author_facet | Luo, Dan Jin, Bin Zhai, Xiangyu Li, Jing Liu, Chuanyong Guo, Wei Li, Jingxin |
author_sort | Luo, Dan |
collection | PubMed |
description | Liver aging impairs the ability of hepatocyte regeneration. Recent studies have found that oxytocin (OT) plays an important role in promoting tissue repair and maintaining differentiation and regeneration of stem cells. Here, we reported that OT receptors, which are specifically located in hepatocytes, decrease with aging in human and mice. Interestingly, the level of serum OT also decline with age. Notably, OT promotes hepatocyte regeneration only in aged mice but not in young mice in vitro and in vivo. Further studies reveal that OT promotes autophagy in either AML12 mouse hepatocytes or aged mice after partial hepatectomy or with CCl4-induced acute liver injury. In conclusion, OT promotes liver regeneration, especially in aged mice, which may be achieved by promoting autophagy. All these results support the possibility of OT and its analog being a potent anti-aging drug and promote liver rejuvenation. |
format | Online Article Text |
id | pubmed-7895748 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-78957482021-03-02 Oxytocin promotes hepatic regeneration in elderly mice Luo, Dan Jin, Bin Zhai, Xiangyu Li, Jing Liu, Chuanyong Guo, Wei Li, Jingxin iScience Article Liver aging impairs the ability of hepatocyte regeneration. Recent studies have found that oxytocin (OT) plays an important role in promoting tissue repair and maintaining differentiation and regeneration of stem cells. Here, we reported that OT receptors, which are specifically located in hepatocytes, decrease with aging in human and mice. Interestingly, the level of serum OT also decline with age. Notably, OT promotes hepatocyte regeneration only in aged mice but not in young mice in vitro and in vivo. Further studies reveal that OT promotes autophagy in either AML12 mouse hepatocytes or aged mice after partial hepatectomy or with CCl4-induced acute liver injury. In conclusion, OT promotes liver regeneration, especially in aged mice, which may be achieved by promoting autophagy. All these results support the possibility of OT and its analog being a potent anti-aging drug and promote liver rejuvenation. Elsevier 2021-02-02 /pmc/articles/PMC7895748/ /pubmed/33659883 http://dx.doi.org/10.1016/j.isci.2021.102125 Text en © 2021 The Author(s) http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Article Luo, Dan Jin, Bin Zhai, Xiangyu Li, Jing Liu, Chuanyong Guo, Wei Li, Jingxin Oxytocin promotes hepatic regeneration in elderly mice |
title | Oxytocin promotes hepatic regeneration in elderly mice |
title_full | Oxytocin promotes hepatic regeneration in elderly mice |
title_fullStr | Oxytocin promotes hepatic regeneration in elderly mice |
title_full_unstemmed | Oxytocin promotes hepatic regeneration in elderly mice |
title_short | Oxytocin promotes hepatic regeneration in elderly mice |
title_sort | oxytocin promotes hepatic regeneration in elderly mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7895748/ https://www.ncbi.nlm.nih.gov/pubmed/33659883 http://dx.doi.org/10.1016/j.isci.2021.102125 |
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