ArticleArteriosclerosis, thrombosis, and vascular biology2023
CD45 Is Sufficient to Initiate Endothelial-to-Mesenchymal Transition in Human Endothelial Cells-Brief Report.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Common Coronary Artery Disease Risk Variants in Endothelial Regulatory Elements Modulate Tetraspanin 14 Expression and Notch Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Endothelial to mesenchymal transition in cardiovascular diseases: molecular insights and clinical perspectives.European heart journal · 2026Review
- Defining the vascular niche of human adipose tissue across metabolic states.Nature metabolism · 2026Article
- Targeting mechanosensitive cannabinoid receptor 1 with isoflavone prodrugs attenuates atherosclerotic endothelial dysfunction.Journal of biomedical science · 2026Article
- New insights into the mechanism of microvascular rarefaction via endothelial-mesenchymal transition in steroid-induced osteonecrosis of femoral head.Scientific reports · 2025Article
- Research advances in epigenetic modifications and post-translational modifications in endothelial-mesenchymal transition.Epigenetics & chromatin · 2025Review
- Defining the vascular niche of human adipose tissue across metabolic states.bioRxiv : the preprint server for biology · 2025Article
- Characterizing SV40-hTERT Immortalized Human Lung Microvascular Endothelial Cells as Model System for Mechanical Stretch-Induced Lung Injury.International journal of molecular sciences · 2025Article
- Novel Role of Endothelial CD45 in Regulating Endothelial-to-Mesenchymal Transition in Atherosclerosis.bioRxiv : the preprint server for biology · 2024Article
- Endothelial Immunosuppression in Atherosclerosis : Translational Control by Elavl1/HuR.bioRxiv : the preprint server for biology · 2024Article
- Recent advances in endothelial colony-forming cells: from the transcriptomic perspective.Journal of translational medicine · 2024Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEndothelial-to-mesenchymal transition (EndMT) is a dynamic process in which endothelial cells acquire mesenchymal properties and in turn contribute to tissue remodeling and growth. Previously, we found EndMT associated with mitral valve adaptation after myocardial infarction. Furthermore, mitral valve endothelial cells collected at 6 months post-myocardial infarction expressed the pan-leukocyte marker CD45 and EndMT markers. Additionally, mitral valve endothelial cells induced to undergo EndMT with TGF (transforming growth factor)-β1 strongly coexpressed CD45 but not CD11b or CD14. Pharmacologic inhibition of the CD45 PTPase (protein tyrosine phosphatase) domain in mitral valve endothelial cells blocked TGFβ-induced EndMT. This prompted us to speculate that, downstream of TGFβ, CD45 induces EndMT.
methodsWe activated the endogenous CD45 promoter in human endothelial colony forming cells (ECFCs) using CRISPR (cluster regularly interspaced short palindromic repeats)/inactive Cas9 (CRISPR-associated protein 9) transcriptional activation. Bulk RNA sequencing was performed on control ECFCs and CD45-positive ECFCs to identify transcriptomic changes. Three functional assays-cellular migration, collagen gel contraction, and transendothelial electrical resistance-were conducted to assess mesenchymal properties in CD45-positive ECFCs.
resultsActivation of the endogenous CD45 promoter in ECFC and 3 additional sources of endothelial cells induced expression of several genes implicated in EndMT. In addition, CD45-positive ECFCs showed increased migration, a hallmark of EndMT, increased collagen gel contraction, a hallmark of mesenchymal cells, and decreased cell-cell barrier integrity, indicating reduced endothelial function.
conclusionsCD45 is sufficient to incite an EndMT phenotype and acquisition of mesenchymal cell properties in normal human ECFCs. We speculate that CD45, through its C-terminal PTPase domain, initiates signaling events that drive EndMT.
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