دورية أكاديمية
Type I Interferons induce endothelial destabilization in Systemic Lupus Erythematosus in a Tie2-dependent manner.
العنوان: | Type I Interferons induce endothelial destabilization in Systemic Lupus Erythematosus in a Tie2-dependent manner. |
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المؤلفون: | Rafael-Vidal C; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain., Martínez-Ramos S; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain., Malvar-Fernández B; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain., Altabás-González I; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain., Mouriño C; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain., Veale DJ; Molecular Rheumatology, Clinical Medicine, Trinity Biomedical Science Institute, Dublin, Ireland.; European Alliance of Associations for Rheumatology (EULAR) Centre for Arthritis and Rheumatic Diseases, St Vincent's University Hospital, University College Dublin, Dublin, Ireland., Floudas A; School of Biotechnology, Dublin City University, Dublin, Ireland., Fearon U; Molecular Rheumatology, Clinical Medicine, Trinity Biomedical Science Institute, Dublin, Ireland.; European Alliance of Associations for Rheumatology (EULAR) Centre for Arthritis and Rheumatic Diseases, St Vincent's University Hospital, University College Dublin, Dublin, Ireland., Reigosa JMP; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain., García S; Rheumatology and Immune-mediated Diseases Group, Galicia Sur Health Research Institute (IIS Galicia Sur), Vigo, Spain.; Rheumatology Department, University Hospital of Vigo, Vigo, Spain. |
المصدر: | Frontiers in immunology [Front Immunol] 2023 Dec 14; Vol. 14, pp. 1277267. Date of Electronic Publication: 2023 Dec 14 (Print Publication: 2023). |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE |
أسماء مطبوعة: | Original Publication: [Lausanne : Frontiers Research Foundation] |
مواضيع طبية MeSH: | Interferon Type I*/pharmacology , Lupus Erythematosus, Systemic* , Receptor, TIE-2*/metabolism, Humans ; Human Umbilical Vein Endothelial Cells/metabolism ; Signal Transduction |
مستخلص: | Endothelial cell (EC) dysfunction is a hallmark of Systemic Lupus Erythematosus (SLE) and Tie2 is a receptor essential for vascular stability. Inflammatory processes promote inhibition of Tie2 homeostatic activation, driving vascular dysfunction. In this work we determined whether type I Interferons (IFN) induce Tie2 signalling-mediated endothelial dysfunction in patients with SLE. Serum levels of Angiopoietin (Ang)-1, Ang-2 and soluble (s)Tie1 in patients with SLE and healthy controls were measured by ELISA. Monocytes from patients with SLE and Human Umbilical Vein EC (HUVEC) were stimulated with IFN-α, IFN-β (1000 I.U.) or SLE serum (20%). mRNA and protein expression, phosphorylation and translocation were determined by quantitative PCR, ELISA, Western Blot, flow cytometry and confocal microscopy. Viability and angiogenic capacity were determined by calcein and tube formation assays. We found that sTie1 and Ang-2 serum levels were increased and Ang-1 decreased in patients with SLE and were associated with clinical characteristics. Type I IFN significantly decreased Ang-1 and increased Ang-2 in monocytes from patients with SLE. Type I IFN increased sTie1 and Ang-2 secretion and reduced Tie2 activation in HUVEC. Functionally, type I IFN significantly reduced EC viability and impaired angiogenesis in a Tie2 signalling-dependent manner. Finally, SLE serum increased Ang-2 and sTie1 secretion and significantly decreased tube formation. Importantly, Tie1 and IFNAR1 knockdown reversed these effects in tube formation. Overall, type I IFN play an important role in the stability of EC by inhibiting Tie2 signalling, suggesting that these processes may be implicated in the cardiovascular events observed in patients with SLE. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Rafael-Vidal, Martínez-Ramos, Malvar-Fernández, Altabás-González, Mouriño, Veale, Floudas, Fearon, Reigosa and García.) |
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فهرسة مساهمة: | Keywords: Tie2; angiopoietins; cardiovascular risk; endothelial destabilization; systemic lupus erythematosus; type I interferons |
سلسلة جزيئية: | GEO GSE173767; GSE157293; GSE112943 |
المشرفين على المادة: | 0 (Interferon Type I) EC 2.7.10.1 (Receptor, TIE-2) EC 2.7.10.1 (TEK protein, human) |
تواريخ الأحداث: | Date Created: 20240101 Date Completed: 20240103 Latest Revision: 20240325 |
رمز التحديث: | 20240326 |
مُعرف محوري في PubMed: | PMC10756137 |
DOI: | 10.3389/fimmu.2023.1277267 |
PMID: | 38162654 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1664-3224 |
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DOI: | 10.3389/fimmu.2023.1277267 |