Cargando…
MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway
MARCH5 is a critical regulator of mitochondrial dynamics, apoptosis and mitophagy. However, its role in cardiovascular system remains poorly understood. This study aimed to investigate the role of MARCH5 in endothelial cell (ECs) injury and the involvement of the Akt/eNOS signalling pathway in this...
Autores principales: | , , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8034466/ https://www.ncbi.nlm.nih.gov/pubmed/33611830 http://dx.doi.org/10.1111/jcmm.16386 |
_version_ | 1783676550306070528 |
---|---|
author | Lei, Wenhua Li, Junli Li, Changming Chen, Li Huang, Fangyang Xiao, Dan Zhang, Jialiang Zhao, Jiahao Li, Guoyong Qu, Tianyi Zhou, Hao Liao, Yanbiao Chen, Mao |
author_facet | Lei, Wenhua Li, Junli Li, Changming Chen, Li Huang, Fangyang Xiao, Dan Zhang, Jialiang Zhao, Jiahao Li, Guoyong Qu, Tianyi Zhou, Hao Liao, Yanbiao Chen, Mao |
author_sort | Lei, Wenhua |
collection | PubMed |
description | MARCH5 is a critical regulator of mitochondrial dynamics, apoptosis and mitophagy. However, its role in cardiovascular system remains poorly understood. This study aimed to investigate the role of MARCH5 in endothelial cell (ECs) injury and the involvement of the Akt/eNOS signalling pathway in this process. Rat models of myocardial infarction (MI) and human cardiac microvascular endothelial cells (HCMECs) exposed to hypoxia (1% O(2)) were used in this study. MARCH5 expression was significantly reduced in ECs of MI hearts and ECs exposed to hypoxia. Hypoxia inhibited the proliferation, migration and tube formation of ECs, and these effects were aggravated by knockdown of MARCH5 but antagonized by overexpressed MARCH5. Overexpression of MARCH5 increased nitric oxide (NO) content, p‐eNOS and p‐Akt, while MARCH5 knockdown exerted the opposite effects. The protective effects mediated by MARCH5 overexpression on ECs could be inhibited by eNOS inhibitor L‐NAME and Akt inhibitor LY294002. In conclusion, these results indicated that MARCH5 acts as a protective factor in ischaemia/hypoxia‐induced ECs injury partially through Akt/eNOS pathway. |
format | Online Article Text |
id | pubmed-8034466 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-80344662021-04-14 MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway Lei, Wenhua Li, Junli Li, Changming Chen, Li Huang, Fangyang Xiao, Dan Zhang, Jialiang Zhao, Jiahao Li, Guoyong Qu, Tianyi Zhou, Hao Liao, Yanbiao Chen, Mao J Cell Mol Med Original Articles MARCH5 is a critical regulator of mitochondrial dynamics, apoptosis and mitophagy. However, its role in cardiovascular system remains poorly understood. This study aimed to investigate the role of MARCH5 in endothelial cell (ECs) injury and the involvement of the Akt/eNOS signalling pathway in this process. Rat models of myocardial infarction (MI) and human cardiac microvascular endothelial cells (HCMECs) exposed to hypoxia (1% O(2)) were used in this study. MARCH5 expression was significantly reduced in ECs of MI hearts and ECs exposed to hypoxia. Hypoxia inhibited the proliferation, migration and tube formation of ECs, and these effects were aggravated by knockdown of MARCH5 but antagonized by overexpressed MARCH5. Overexpression of MARCH5 increased nitric oxide (NO) content, p‐eNOS and p‐Akt, while MARCH5 knockdown exerted the opposite effects. The protective effects mediated by MARCH5 overexpression on ECs could be inhibited by eNOS inhibitor L‐NAME and Akt inhibitor LY294002. In conclusion, these results indicated that MARCH5 acts as a protective factor in ischaemia/hypoxia‐induced ECs injury partially through Akt/eNOS pathway. John Wiley and Sons Inc. 2021-02-21 2021-04 /pmc/articles/PMC8034466/ /pubmed/33611830 http://dx.doi.org/10.1111/jcmm.16386 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Lei, Wenhua Li, Junli Li, Changming Chen, Li Huang, Fangyang Xiao, Dan Zhang, Jialiang Zhao, Jiahao Li, Guoyong Qu, Tianyi Zhou, Hao Liao, Yanbiao Chen, Mao MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title | MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title_full | MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title_fullStr | MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title_full_unstemmed | MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title_short | MARCH5 restores endothelial cell function against ischaemic/hypoxia injury via Akt/eNOS pathway |
title_sort | march5 restores endothelial cell function against ischaemic/hypoxia injury via akt/enos pathway |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8034466/ https://www.ncbi.nlm.nih.gov/pubmed/33611830 http://dx.doi.org/10.1111/jcmm.16386 |
work_keys_str_mv | AT leiwenhua march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT lijunli march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT lichangming march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT chenli march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT huangfangyang march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT xiaodan march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT zhangjialiang march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT zhaojiahao march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT liguoyong march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT qutianyi march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT zhouhao march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT liaoyanbiao march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway AT chenmao march5restoresendothelialcellfunctionagainstischaemichypoxiainjuryviaaktenospathway |