Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension

Background Hypoxia‐induced pulmonary hypertension (HPH) is a severe vascular disorder that is characterized by the involvement of endothelial‐to‐mesenchymal transition (EndMT) in its pathogenesis. Our previous research has suggested that the gene versican may have a crucial role in the development o...

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Main Authors: Jinyan Yu, Shanchao Hong, Lingjia Yang, Shugao Ye, Zhen Yu, Zheming Zhang, Ziteng Wang, Shulun Huang, Yuan Chen, Tao Bian, Yan Wu
Format: Article
Language:English
Published: Wiley 2024-12-01
Series:Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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Online Access:https://www.ahajournals.org/doi/10.1161/JAHA.124.036969
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author Jinyan Yu
Shanchao Hong
Lingjia Yang
Shugao Ye
Zhen Yu
Zheming Zhang
Ziteng Wang
Shulun Huang
Yuan Chen
Tao Bian
Yan Wu
author_facet Jinyan Yu
Shanchao Hong
Lingjia Yang
Shugao Ye
Zhen Yu
Zheming Zhang
Ziteng Wang
Shulun Huang
Yuan Chen
Tao Bian
Yan Wu
author_sort Jinyan Yu
collection DOAJ
description Background Hypoxia‐induced pulmonary hypertension (HPH) is a severe vascular disorder that is characterized by the involvement of endothelial‐to‐mesenchymal transition (EndMT) in its pathogenesis. Our previous research has suggested that the gene versican may have a crucial role in the development of HPH. However, the exact function of versican in HPH requires further investigation. Methods and Results The expression of versican and markers of EndMT was assessed using Western blot, immunohistochemistry, and immunofluorescence. Vascular remodeling and right ventricular hypertrophy in patients with HPH and mice were evaluated through hematoxylin and eosin staining, Masson's staining, and hemodynamic measurements. Protein interactions were validated using co‐immunoprecipitation, and the DNA methylation level of versican was examined using methylation‐specific polymerase chain reaction. Compared with the control, EndMT was observed in patients with HPH, HPH mouse models, and hypoxia‐treated human pulmonary artery endothelial cells, accompanied by a significant increase of versican. Endothelium‐specific knockdown of versican reversed HPH progression and effectively prevented EndMT in mouse models and human pulmonary artery endothelial cells. We further confirmed that versican participated in EndMT by targeting the key transcription factor Twist1. Additionally, the upregulation of versican may be attributed to promoter hypomethylation, which was mediated by reduced DNA methyltransferases activity under hypoxic conditions. Conclusions This study provides the initial evidence showcasing the role of promoter hypomethylation‐mediated versican upregulation in promoting EndMT by targeting Twist1, which facilitates vascular remodeling and the progression of HPH. These findings offer a promising new target for the treatment of HPH.
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spelling doaj-art-1c3fd786d0ae4f5997c7362798e1d55d2025-08-20T02:50:40ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802024-12-01132310.1161/JAHA.124.036969Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary HypertensionJinyan Yu0Shanchao Hong1Lingjia Yang2Shugao Ye3Zhen Yu4Zheming Zhang5Ziteng Wang6Shulun Huang7Yuan Chen8Tao Bian9Yan Wu10Department of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Clinical Laboratory Jiangnan University Medical Center Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaTransplant Center The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaTransplant Center The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaDepartment of Respiratory Medicine The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University Wuxi Jiangsu People’s Republic of ChinaBackground Hypoxia‐induced pulmonary hypertension (HPH) is a severe vascular disorder that is characterized by the involvement of endothelial‐to‐mesenchymal transition (EndMT) in its pathogenesis. Our previous research has suggested that the gene versican may have a crucial role in the development of HPH. However, the exact function of versican in HPH requires further investigation. Methods and Results The expression of versican and markers of EndMT was assessed using Western blot, immunohistochemistry, and immunofluorescence. Vascular remodeling and right ventricular hypertrophy in patients with HPH and mice were evaluated through hematoxylin and eosin staining, Masson's staining, and hemodynamic measurements. Protein interactions were validated using co‐immunoprecipitation, and the DNA methylation level of versican was examined using methylation‐specific polymerase chain reaction. Compared with the control, EndMT was observed in patients with HPH, HPH mouse models, and hypoxia‐treated human pulmonary artery endothelial cells, accompanied by a significant increase of versican. Endothelium‐specific knockdown of versican reversed HPH progression and effectively prevented EndMT in mouse models and human pulmonary artery endothelial cells. We further confirmed that versican participated in EndMT by targeting the key transcription factor Twist1. Additionally, the upregulation of versican may be attributed to promoter hypomethylation, which was mediated by reduced DNA methyltransferases activity under hypoxic conditions. Conclusions This study provides the initial evidence showcasing the role of promoter hypomethylation‐mediated versican upregulation in promoting EndMT by targeting Twist1, which facilitates vascular remodeling and the progression of HPH. These findings offer a promising new target for the treatment of HPH.https://www.ahajournals.org/doi/10.1161/JAHA.124.036969DNA methylationendothelial‐to‐mesenchymal transitionhypoxia‐induced pulmonary hypertensionTwist1versican
spellingShingle Jinyan Yu
Shanchao Hong
Lingjia Yang
Shugao Ye
Zhen Yu
Zheming Zhang
Ziteng Wang
Shulun Huang
Yuan Chen
Tao Bian
Yan Wu
Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
DNA methylation
endothelial‐to‐mesenchymal transition
hypoxia‐induced pulmonary hypertension
Twist1
versican
title Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
title_full Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
title_fullStr Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
title_full_unstemmed Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
title_short Promotor Hypomethylation Mediated Upregulation of VCAN Targets Twist1 to Promote EndMT in Hypoxia‐Induced Pulmonary Hypertension
title_sort promotor hypomethylation mediated upregulation of vcan targets twist1 to promote endmt in hypoxia induced pulmonary hypertension
topic DNA methylation
endothelial‐to‐mesenchymal transition
hypoxia‐induced pulmonary hypertension
Twist1
versican
url https://www.ahajournals.org/doi/10.1161/JAHA.124.036969
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