Cargando…
miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction
Homocysteine (Hcy) is a risk factor for multiple chronic diseases, and vascular endothelial cell injury has been regarded as the initiating step for this process. miRNAs are involved in Hcy-induced endothelial dysfunction, while the underlying mechanism and roles of miRNAs in pulmonary endothelial d...
Autores principales: | , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10520487/ https://www.ncbi.nlm.nih.gov/pubmed/37491880 http://dx.doi.org/10.3724/abbs.2023127 |
_version_ | 1785109930476306432 |
---|---|
author | Huang, Xiaobo Li, Zhen Zhang, Ling Yang, Yali Wang, Yanjia Li, Sirui Li, Guizhong Feng, Huiping Yang, Xiaoling |
author_facet | Huang, Xiaobo Li, Zhen Zhang, Ling Yang, Yali Wang, Yanjia Li, Sirui Li, Guizhong Feng, Huiping Yang, Xiaoling |
author_sort | Huang, Xiaobo |
collection | PubMed |
description | Homocysteine (Hcy) is a risk factor for multiple chronic diseases, and vascular endothelial cell injury has been regarded as the initiating step for this process. miRNAs are involved in Hcy-induced endothelial dysfunction, while the underlying mechanism and roles of miRNAs in pulmonary endothelial dysfunction induced by homocysteine are unknown. Here, we find that miR-205-5p alleviates pulmonary endothelial dysfunction by targeting FOXO1 in CBS (+/‒) mice to protect against Hcy-induced pulmonary endothelial dysfunction. Mechanistically, we show that Hcy can lead to DNA hypermethylation of the miR-205-5p promoter due to the increased binding of DNMT1 to its promoter, which contributes to reduction of miR-205-5p expression. In summary, miR-205-5p promoter hypermethylation causes downregulation of miR-205-5p expression, resulting in a reduction in miR-205-5p binding to FOXO1 during homocysteine-induced pulmonary endothelial dysfunction. Our data indicate that miR-205-5p may be a potential therapeutic target against Hcy-induced pulmonary injury. |
format | Online Article Text |
id | pubmed-10520487 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-105204872023-09-27 miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction Huang, Xiaobo Li, Zhen Zhang, Ling Yang, Yali Wang, Yanjia Li, Sirui Li, Guizhong Feng, Huiping Yang, Xiaoling Acta Biochim Biophys Sin (Shanghai) Research Article Homocysteine (Hcy) is a risk factor for multiple chronic diseases, and vascular endothelial cell injury has been regarded as the initiating step for this process. miRNAs are involved in Hcy-induced endothelial dysfunction, while the underlying mechanism and roles of miRNAs in pulmonary endothelial dysfunction induced by homocysteine are unknown. Here, we find that miR-205-5p alleviates pulmonary endothelial dysfunction by targeting FOXO1 in CBS (+/‒) mice to protect against Hcy-induced pulmonary endothelial dysfunction. Mechanistically, we show that Hcy can lead to DNA hypermethylation of the miR-205-5p promoter due to the increased binding of DNMT1 to its promoter, which contributes to reduction of miR-205-5p expression. In summary, miR-205-5p promoter hypermethylation causes downregulation of miR-205-5p expression, resulting in a reduction in miR-205-5p binding to FOXO1 during homocysteine-induced pulmonary endothelial dysfunction. Our data indicate that miR-205-5p may be a potential therapeutic target against Hcy-induced pulmonary injury. Oxford University Press 2023-07-25 /pmc/articles/PMC10520487/ /pubmed/37491880 http://dx.doi.org/10.3724/abbs.2023127 Text en © The Author(s) 2021. 0 https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Research Article Huang, Xiaobo Li, Zhen Zhang, Ling Yang, Yali Wang, Yanjia Li, Sirui Li, Guizhong Feng, Huiping Yang, Xiaoling miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title | miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title_full | miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title_fullStr | miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title_full_unstemmed | miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title_short | miR-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting FOXO1: miR-205-5p inhibits pulmonary microvascular endothelial dysfunction |
title_sort | mir-205-5p inhibits homocysteine-induced pulmonary microvascular endothelium dysfunction by targeting foxo1: mir-205-5p inhibits pulmonary microvascular endothelial dysfunction |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10520487/ https://www.ncbi.nlm.nih.gov/pubmed/37491880 http://dx.doi.org/10.3724/abbs.2023127 |
work_keys_str_mv | AT huangxiaobo mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT lizhen mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT zhangling mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT yangyali mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT wangyanjia mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT lisirui mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT liguizhong mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT fenghuiping mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction AT yangxiaoling mir2055pinhibitshomocysteineinducedpulmonarymicrovascularendotheliumdysfunctionbytargetingfoxo1mir2055pinhibitspulmonarymicrovascularendothelialdysfunction |