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The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2

COVID-19, a novel identified coronavirus disease due to Severe Acute Respiratory Syndrome coronaviruses 2 (SARS-Cov-2) infection, has posed a significant threat to public health worldwide. It has been reported COVID-19 keeps substantial nucleotide similarity and shares common receptor, Angiotensin-c...

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Autores principales: Luo, Jing, Lu, Saisai, Yu, Mengjiao, Zhu, Lixia, Zhu, Chengwei, Li, Chenlu, Fang, Jinxia, Zhu, Xiaochun, Wang, Xiaobing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier B.V. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695578/
https://www.ncbi.nlm.nih.gov/pubmed/33253796
http://dx.doi.org/10.1016/j.gene.2020.145325
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author Luo, Jing
Lu, Saisai
Yu, Mengjiao
Zhu, Lixia
Zhu, Chengwei
Li, Chenlu
Fang, Jinxia
Zhu, Xiaochun
Wang, Xiaobing
author_facet Luo, Jing
Lu, Saisai
Yu, Mengjiao
Zhu, Lixia
Zhu, Chengwei
Li, Chenlu
Fang, Jinxia
Zhu, Xiaochun
Wang, Xiaobing
author_sort Luo, Jing
collection PubMed
description COVID-19, a novel identified coronavirus disease due to Severe Acute Respiratory Syndrome coronaviruses 2 (SARS-Cov-2) infection, has posed a significant threat to public health worldwide. It has been reported COVID-19 keeps substantial nucleotide similarity and shares common receptor, Angiotensin-converting enzyme 2 (ACE2) with Severe Acute Respiratory Syndrome coronaviruses (SARS-Cov). Here, we investigated the gene expression of ACE2 and identified associated pathways of SARS-Cov as a useful reference for a deepening understanding of COVID-19. The results indicated the ACE2 was overexpressed in human airway epithelial cells (HAEs), especially at 72 h after SARS-Cov infection. We found ACE2 might regulate immune response through immunological activation-associated pathways in the process of in both SARS-Cov and SARS-Cov-2 infection, where the activation of B cells, macrophages, helper T cells 1 (Th1 cells) and the inhibition of Foxp3 + regulatory T (Treg) cells and CD8 + T cells were found to be prominent. Finally, significant correlation between ACE2 and JAK-STAT signaling pathway was identified which indicate that JAK-STAT signaling pathway might involve in the downstream action of the overactivation of ACE2. These findings are expected to gain a further insight into the action mechanism of COVID-19 infection and provide a promising target for designing effective therapeutic strategies.
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spelling pubmed-76955782020-12-01 The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2 Luo, Jing Lu, Saisai Yu, Mengjiao Zhu, Lixia Zhu, Chengwei Li, Chenlu Fang, Jinxia Zhu, Xiaochun Wang, Xiaobing Gene Research Paper COVID-19, a novel identified coronavirus disease due to Severe Acute Respiratory Syndrome coronaviruses 2 (SARS-Cov-2) infection, has posed a significant threat to public health worldwide. It has been reported COVID-19 keeps substantial nucleotide similarity and shares common receptor, Angiotensin-converting enzyme 2 (ACE2) with Severe Acute Respiratory Syndrome coronaviruses (SARS-Cov). Here, we investigated the gene expression of ACE2 and identified associated pathways of SARS-Cov as a useful reference for a deepening understanding of COVID-19. The results indicated the ACE2 was overexpressed in human airway epithelial cells (HAEs), especially at 72 h after SARS-Cov infection. We found ACE2 might regulate immune response through immunological activation-associated pathways in the process of in both SARS-Cov and SARS-Cov-2 infection, where the activation of B cells, macrophages, helper T cells 1 (Th1 cells) and the inhibition of Foxp3 + regulatory T (Treg) cells and CD8 + T cells were found to be prominent. Finally, significant correlation between ACE2 and JAK-STAT signaling pathway was identified which indicate that JAK-STAT signaling pathway might involve in the downstream action of the overactivation of ACE2. These findings are expected to gain a further insight into the action mechanism of COVID-19 infection and provide a promising target for designing effective therapeutic strategies. Elsevier B.V. 2021-02-05 2020-11-28 /pmc/articles/PMC7695578/ /pubmed/33253796 http://dx.doi.org/10.1016/j.gene.2020.145325 Text en © 2020 Elsevier B.V. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Research Paper
Luo, Jing
Lu, Saisai
Yu, Mengjiao
Zhu, Lixia
Zhu, Chengwei
Li, Chenlu
Fang, Jinxia
Zhu, Xiaochun
Wang, Xiaobing
The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title_full The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title_fullStr The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title_full_unstemmed The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title_short The potential involvement of JAK-STAT signaling pathway in the COVID-19 infection assisted by ACE2
title_sort potential involvement of jak-stat signaling pathway in the covid-19 infection assisted by ace2
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7695578/
https://www.ncbi.nlm.nih.gov/pubmed/33253796
http://dx.doi.org/10.1016/j.gene.2020.145325
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