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Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation

Interactions between human cytomegalovirus (HCMV) infection and environmental factors can increase susceptibility to essential hypertension (EH). Although endothelial dysfunction is the initial factor of EH, the epigenetic mechanisms through which HCMV infection induces endothelial cell dysfunction...

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Autores principales: Zhang, Xiaoni, Tang, Na, Xi, Dongmei, Feng, Qian, Liu, Yongmin, Wang, Lamei, Tang, Yan, Zhong, Hua, He, Fang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7010708/
https://www.ncbi.nlm.nih.gov/pubmed/32041970
http://dx.doi.org/10.1038/s41598-020-58680-6
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author Zhang, Xiaoni
Tang, Na
Xi, Dongmei
Feng, Qian
Liu, Yongmin
Wang, Lamei
Tang, Yan
Zhong, Hua
He, Fang
author_facet Zhang, Xiaoni
Tang, Na
Xi, Dongmei
Feng, Qian
Liu, Yongmin
Wang, Lamei
Tang, Yan
Zhong, Hua
He, Fang
author_sort Zhang, Xiaoni
collection PubMed
description Interactions between human cytomegalovirus (HCMV) infection and environmental factors can increase susceptibility to essential hypertension (EH). Although endothelial dysfunction is the initial factor of EH, the epigenetic mechanisms through which HCMV infection induces endothelial cell dysfunction are poorly understood. Here, we evaluated whether HCMV regulated endothelial cell function and assessed the underlying mechanisms. Microarray analysis in human umbilical vein endothelial cells (HUVECs) treated with HCMV AD169 strain in the presence of hyperglycemia and hyperlipidemia revealed differential expression of genes involved in hypertension. Further analyses validated that the regulator of G-protein signaling 5 (RGS5) gene was downregulated in infected HUVECs and showed that HCMV infection promoted HUVEC proliferation, whereas hyperglycemia and hyperlipidemia inhibited HUVEC proliferation. Additionally, treatment with decitabine (DAC) and RGS5 reversed the effects of HCMV infection on HUVEC proliferation, but not triggered by hyperglycemia and hyperlipidemia. In summary, upregulation of RGS5 may be a promising treatment for preventing HCMV-induced hypertension.
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spelling pubmed-70107082020-02-21 Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation Zhang, Xiaoni Tang, Na Xi, Dongmei Feng, Qian Liu, Yongmin Wang, Lamei Tang, Yan Zhong, Hua He, Fang Sci Rep Article Interactions between human cytomegalovirus (HCMV) infection and environmental factors can increase susceptibility to essential hypertension (EH). Although endothelial dysfunction is the initial factor of EH, the epigenetic mechanisms through which HCMV infection induces endothelial cell dysfunction are poorly understood. Here, we evaluated whether HCMV regulated endothelial cell function and assessed the underlying mechanisms. Microarray analysis in human umbilical vein endothelial cells (HUVECs) treated with HCMV AD169 strain in the presence of hyperglycemia and hyperlipidemia revealed differential expression of genes involved in hypertension. Further analyses validated that the regulator of G-protein signaling 5 (RGS5) gene was downregulated in infected HUVECs and showed that HCMV infection promoted HUVEC proliferation, whereas hyperglycemia and hyperlipidemia inhibited HUVEC proliferation. Additionally, treatment with decitabine (DAC) and RGS5 reversed the effects of HCMV infection on HUVEC proliferation, but not triggered by hyperglycemia and hyperlipidemia. In summary, upregulation of RGS5 may be a promising treatment for preventing HCMV-induced hypertension. Nature Publishing Group UK 2020-02-10 /pmc/articles/PMC7010708/ /pubmed/32041970 http://dx.doi.org/10.1038/s41598-020-58680-6 Text en © The Author(s) 2020 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/.
spellingShingle Article
Zhang, Xiaoni
Tang, Na
Xi, Dongmei
Feng, Qian
Liu, Yongmin
Wang, Lamei
Tang, Yan
Zhong, Hua
He, Fang
Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title_full Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title_fullStr Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title_full_unstemmed Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title_short Human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of G-protein signaling 5 hypermethylation and downregulation
title_sort human cytomegalovirus promoting endothelial cell proliferation by targeting regulator of g-protein signaling 5 hypermethylation and downregulation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7010708/
https://www.ncbi.nlm.nih.gov/pubmed/32041970
http://dx.doi.org/10.1038/s41598-020-58680-6
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