ArticleScientific reports2017
Transcriptome analysis of inflammation-related gene expression in endothelial cells activated by complement MASP-1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- RNA Sequencing and Targeted Knockdown Reveal miR-142a-5p as a Driver of Retinal Degeneration in rd1 Mice.Biology · 2026Article
- Detrimental interactions of hypoxia and complement MASP-1 in endothelial cells as a model for atherosclerosis-related diseases.Scientific reports · 2024Article
- Exercise to Prevent Accelerated Vascular Aging in People Living With HIV.Circulation research · 2024Review
- Complement MASP-1 Modifies Endothelial Wound Healing.International journal of molecular sciences · 2024Article
- Cooperation of Complement MASP-1 with Other Proinflammatory Factors to Enhance the Activation of Endothelial Cells.International journal of molecular sciences · 2023Article
- Review
- Identification of a Prognostic Model Based on Fatty Acid Metabolism-Related Genes of Head and Neck Squamous Cell Carcinoma.Frontiers in genetics · 2022Article
- Molecular Dambusters: What Is Behind Hyperpermeability in Bradykinin-Mediated Angioedema?Clinical reviews in allergy & immunology · 2021Review
- Mitochondrial contributions to vascular endothelial dysfunction, arterial stiffness, and cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2021Review
- Review
- The Influence of the Lectin Pathway of Complement Activation on Infections of the Respiratory System.Frontiers in immunology · 2020Review
- MASP-1 Increases Endothelial Permeability.Frontiers in immunology · 2019Article
- Be on Target: Strategies of Targeting Alternative and Lectin Pathway Components in Complement-Mediated Diseases.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mannan-binding lectin-associated serine protease 1 (MASP-1), the most abundant enzyme of the complement lectin pathway, is able to stimulate human umbilical vein endothelial cells (HUVECs) to alter the expression of several cytokines and adhesion molecules. This study has assessed to what extent MASP-1 is able to modify the transcriptional pattern of inflammation-related (IR) genes in HUVECs. We utilized Agilent microarray to analyse the effects of recombinant MASP-1 (rMASP-1) in HUVECs, on a set of 884 IR genes. Gene Set Enrichment Analysis showed an overall activation of inflammation-related genes in response to rMASP-1. rMASP-1 treatment up- and down-regulated 19 and 11 IR genes, respectively. Most of them were previously unidentified, such as genes of chemokines (CXCL1, CXCL2, CXCL3), inflammatory receptors (TLR2, BDKRB2) and other inflammatory factors (F3, LBP). Expression of IR genes changed early, during the first 2 hours of activation. Both p38-MAPK inhibitor and NFκB inhibitor efficiently suppressed the effect of rMASP-1. We delineated 12 transcriptional factors as possible regulators of rMASP-1-induced IR genes. Our microarray-based data are in line with the hypothesis that complement lectin pathway activation, generating active MASP-1, directly regulates inflammatory processes by shifting the phenotype of endothelial cells towards a more pro-inflammatory type.
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