ArticleFrontiers in cell and developmental biology2022
Upregulation of Neogenin-1 by a CREB1-BAF47 Complex in Vascular Endothelial Cells is Implicated in Atherogenesis.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- NEO1 modulates the A1 astrocyte polarization in subarachnoid hemorrhage through the cPLA2-MAVS signaling pathway.Journal of neuroinflammation · 2025Article
- Identification of potential biomarkers of triton WR-1339 induced hyperlipidemia: NMR-based plasma metabolomics approach and gene expression analysis.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Article
- Superfamily II helicases: the potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Lysophosphatidic Acid Is a Proinflammatory Stimulus of Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- A construction and comprehensive analysis of the immune-related core ceRNA network and infiltrating immune cells in peripheral arterial occlusive disease.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is generally considered a human pathology of chronic inflammation, to which endothelial dysfunction plays an important role. Here we investigated the role of neogenin 1 (Neo-1) in oxidized low-density lipoprotein (oxLDL) induced endothelial dysfunction focusing on its transcriptional regulation. We report that Neo-1 expression was upregulated by oxLDL in both immortalized vascular endothelial cells and primary aortic endothelial cells. Neo-1 knockdown attenuated whereas Neo-1 over-expression enhanced oxLDL-induced leukocyte adhesion to endothelial cells. Neo-1 regulated endothelial-leukocyte interaction by modulating nuclear factor kappa B (NF-κB) activity to alter the expression of adhesion molecules. Neo-1 blockade with a blocking antibody ameliorated atherogenesis in
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