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Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia

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Title: Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia
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
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  Data: Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia
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  Data: <searchLink fieldCode="AR" term="%22Huafang+Wei%22">Huafang Wei</searchLink><br /><searchLink fieldCode="AR" term="%22Lin+Liang%22">Lin Liang</searchLink><br /><searchLink fieldCode="AR" term="%22Chengwen+Song%22">Chengwen Song</searchLink><br /><searchLink fieldCode="AR" term="%22Ming+Tong%22">Ming Tong</searchLink><br /><searchLink fieldCode="AR" term="%22Xiang+Xu%22">Xiang Xu</searchLink>
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  Data: Association of Basic Medical Sciences of Federation of Bosnia and Herzegovina, 2024.
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  Data: 2024
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  Data: LCC:Biology (General)
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  Data: <searchLink fieldCode="DE" term="%22Preeclampsia%22">Preeclampsia</searchLink><br /><searchLink fieldCode="DE" term="%22vascular+endothelial+cell+injury%22">vascular endothelial cell injury</searchLink><br /><searchLink fieldCode="DE" term="%22METTL14%22">METTL14</searchLink><br /><searchLink fieldCode="DE" term="%22miR-34a-5p%22">miR-34a-5p</searchLink><br /><searchLink fieldCode="DE" term="%22FOXP1%22">FOXP1</searchLink><br /><searchLink fieldCode="DE" term="%22m6A+modification%22">m6A modification</searchLink><br /><searchLink fieldCode="DE" term="%22Biology+%28General%29%22">Biology (General)</searchLink><br /><searchLink fieldCode="DE" term="%22QH301-705%2E5%22">QH301-705.5</searchLink>
– Name: Abstract
  Label: Description
  Group: Ab
  Data: 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.
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        Value: 10.17305/bb.2024.10963
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      – Text: English
    Subjects:
      – SubjectFull: Preeclampsia
        Type: general
      – SubjectFull: vascular endothelial cell injury
        Type: general
      – SubjectFull: METTL14
        Type: general
      – SubjectFull: miR-34a-5p
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      – SubjectFull: QH301-705.5
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      – TitleFull: Regulatory role and molecular mechanism of METTL14 in vascular endothelial cell injury in preeclampsia
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