ArticleScientific reports2024
Detrimental interactions of hypoxia and complement MASP-1 in endothelial cells as a model for atherosclerosis-related diseases.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- Activation of the C3a-C3aReceptor-axis is associated with endothelial dysfunction and glycocalyx damage in ST-elevation myocardial infarction.Basic research in cardiology · 2026Article
- Protein Kinase C-Delta (PKCδ) inhibition stabilizes endothelium and suppresses triple-negative breast cancer (TNBC) intravasation in a microfluidic hypoxic tumor model.Bioengineering & translational medicine · 2026Article
- Nature versus nurture: genetic background and media composition shape endothelial cell transcriptomes in vitro.Scientific reports · 2026Article
- Correlation of serum MAp44 protein concentration with degree of myocardial injury and 30-day prognosis in patients with acute myocardial infarction.American journal of translational research · 2026Article
- Study on the Predictive Value of MASP-1 Combined with Four Thrombotic Molecular Markers for Disseminated Intravascular Coagulation in Patients with Severe Infection.Infection and drug resistance · 2025Article
- Complement MASP-1 Modifies Endothelial Wound Healing.International journal of molecular sciences · 2024Article
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Authors and funding
7 authors.
Funding
Abstract
Both hypoxia and the complement lectin pathway (CLP) are involved in atherosclerosis and atherosclerosis-related stroke and acute myocardial infarction (AMI). We have previously shown that mannose-binding lectin-associated serine protease-1 (MASP-1), the most abundant enzyme of CLP, induces an inflammatory phenotype of endothelial cells (ECs) by cleaving protease activated receptors (PARs). In the absence of data, we aimed to investigate whether hypoxia and MASP-1 interact at the level of ECs, to better understand their role in atherosclerosis-related diseases. Hypoxia attenuated the wound healing ability of ECs, increased ICAM-1 and decreased ICAM-2 expression and upregulated PAR2 gene expression. Hypoxia and MASP-1 increased GROα and IL-8 production, and endothelial permeability without potentiating each other's effects, whereas they cooperatively disrupted vascular network integrity, activated the Ca
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