Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53
Angiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of cardiovascular disease. This study aimed to investigate the role of maternally expressed gene 3 (Meg3) in endothelial cell injury. A lncRNA human gene expression microarray analysis was used...
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Frontiers Media S.A.
2019-02-01
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| Series: | Frontiers in Genetics |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fgene.2019.00078/full |
| _version_ | 1818951136936198144 |
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| author | Jingwen Song Songqun Huang Kaizhong Wang Wei Li Lizhi Pao Feng Chen Xianxian Zhao |
| author_facet | Jingwen Song Songqun Huang Kaizhong Wang Wei Li Lizhi Pao Feng Chen Xianxian Zhao |
| author_sort | Jingwen Song |
| collection | DOAJ |
| description | Angiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of cardiovascular disease. This study aimed to investigate the role of maternally expressed gene 3 (Meg3) in endothelial cell injury. A lncRNA human gene expression microarray analysis was used to identify differentially expressed lncRNAs in human umbilical vein endothelial cell (HUVECs). Cell viability, apoptosis, and migration were then assessed Ang II-treated HUVECs. qRT-PCR and western blotting were performed to detect the expression level of p53 after Meg3 knockdown and overexpression. We observed that Ang II treatment decreased the Meg3 level in HUVECs. Next, both knockdown of Meg3 and Ang II decreased cell viability, increased apoptotic cell rate and impair migration function in HUVECs. Furthermore, overexpression of Meg3 inhibited cell apoptosis, and increased cell migration by enhancing p53 transcription on its target genes, including CRP, ICAM-1, VEGF, and HIF-1α. Our findings indicate that Meg3 might be associated with cardiovascular disease development. |
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| institution | Directory Open Access Journal |
| issn | 1664-8021 |
| language | English |
| last_indexed | 2024-12-20T09:29:42Z |
| publishDate | 2019-02-01 |
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| series | Frontiers in Genetics |
| spelling | doaj.art-75d42e3b4dcd462b8cb101b07290f5e52022-12-21T19:45:07ZengFrontiers Media S.A.Frontiers in Genetics1664-80212019-02-011010.3389/fgene.2019.00078423837Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53Jingwen Song0Songqun Huang1Kaizhong Wang2Wei Li3Lizhi Pao4Feng Chen5Xianxian Zhao6Department of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaInstitute of Tumor, Second Military Medical University, Shanghai, ChinaDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaDepartment of Cardiovascularology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, ChinaAngiotensin II (Ang II)-induced damage to endothelial cells (ECs) plays a crucial role in the pathogenesis of cardiovascular disease. This study aimed to investigate the role of maternally expressed gene 3 (Meg3) in endothelial cell injury. A lncRNA human gene expression microarray analysis was used to identify differentially expressed lncRNAs in human umbilical vein endothelial cell (HUVECs). Cell viability, apoptosis, and migration were then assessed Ang II-treated HUVECs. qRT-PCR and western blotting were performed to detect the expression level of p53 after Meg3 knockdown and overexpression. We observed that Ang II treatment decreased the Meg3 level in HUVECs. Next, both knockdown of Meg3 and Ang II decreased cell viability, increased apoptotic cell rate and impair migration function in HUVECs. Furthermore, overexpression of Meg3 inhibited cell apoptosis, and increased cell migration by enhancing p53 transcription on its target genes, including CRP, ICAM-1, VEGF, and HIF-1α. Our findings indicate that Meg3 might be associated with cardiovascular disease development.https://www.frontiersin.org/article/10.3389/fgene.2019.00078/fullcardiovascular diseaseHUVECsAng IIMeg3p53 |
| spellingShingle | Jingwen Song Songqun Huang Kaizhong Wang Wei Li Lizhi Pao Feng Chen Xianxian Zhao Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 Frontiers in Genetics cardiovascular disease HUVECs Ang II Meg3 p53 |
| title | Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 |
| title_full | Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 |
| title_fullStr | Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 |
| title_full_unstemmed | Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 |
| title_short | Long Non-coding RNA MEG3 Attenuates the Angiotensin II-Induced Injury of Human Umbilical Vein Endothelial Cells by Interacting With p53 |
| title_sort | long non coding rna meg3 attenuates the angiotensin ii induced injury of human umbilical vein endothelial cells by interacting with p53 |
| topic | cardiovascular disease HUVECs Ang II Meg3 p53 |
| url | https://www.frontiersin.org/article/10.3389/fgene.2019.00078/full |
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