Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia
| Title: | Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia |
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| Authors: | Huafang Wei, Lin Liang, Chengwen Song, Ming Tong, Xiang Xu |
| Source: | Biomolecules & Biomedicine (2024) |
| Publisher Information: | Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina, 2024. |
| Publication Year: | 2024 |
| Collection: | LCC:Biology (General) |
| Subject Terms: | Preeclampsia, vascular endothelial cell injury, METTL14, miR-34a-5p, FOXP1, m6A modification, Biology (General), QH301-705.5 |
| More Details: | Preeclampsia (PE) is a pregnancy-related disease characterized by vascular endothelial cell injury. This study aimed to investigate the role of methyltransferase-like protein 14 (METTL14) in vascular endothelial cell injury in PE. The PE cell model was established by treating human umbilical vein endothelial cells (HUVECs) with tumor necrosis factor-alpha (TNF-α) in vitro. METTL14 and forkhead box protein 1 (FOXP1) were silenced, and miR-34a-5p was overexpressed in HUVECs to evaluate their effects. HUVEC viability, apoptosis, and the levels of intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and endothelin-1 were measured. The N6-methyladenosine (m6A) modification of pri-miR-34a-5p was quantified. The interactions between miR-34a-5p, DiGeorge syndrome critical region 8, and m6A enrichment in miR-34a-5p were analyzed. The relationship between miR-34a-5p and FOXP1 was also verified. The results showed that the expressions of METTL14, FOXP1, and miR-34a-5p were determined. METTL14 expression was elevated in the TNF-α-induced HUVEC injury model. Silencing METTL14 improved HUVEC viability, inhibited apoptosis, and reduced endothelial inflammation. METTL14 promoted miR-34a-5p expression through m6A modification. Overexpression of miR-34a-5p or silencing of FOXP1 reversed the protective effects of METTL14 silencing on cell injury in the PE model. In conclusion, METTL14 mediated m6A modification to promote miR-34a-5p expression, leading to the inhibition of FOXP1 expression, which aggravated endothelial cell damage in the PE cell model. |
| Document Type: | article |
| File Description: | electronic resource |
| Language: | English |
| ISSN: | 2831-0896 2831-090X |
| Relation: | https://www.bjbms.org/ojs/index.php/bjbms/article/view/10963; https://doaj.org/toc/2831-0896; https://doaj.org/toc/2831-090X |
| DOI: | 10.17305/bb.2024.10963 |
| Access URL: | https://doaj.org/article/0b02aa578684470b972c9762c451e729 |
| Accession Number: | edsdoj.0b02aa578684470b972c9762c451e729 |
| Database: | Directory of Open Access Journals |
| ISSN: | 28310896 2831090X |
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| DOI: | 10.17305/bb.2024.10963 |
| Published in: | Biomolecules & Biomedicine |
| Language: | English |