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. |
|---|---|
| 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.) |
| References: | PLoS One. 2012;7(5):e37000. (PMID: 22606325) Front Cell Dev Biol. 2021 Feb 16;9:642352. (PMID: 33681228) Cell. 2021 Aug 19;184(17):4464-4479.e19. (PMID: 34384544) Ann Rheum Dis. 2009 Oct;68(10):1638-43. (PMID: 18930996) Immunol Invest. 2012;41(8):864-75. (PMID: 22989097) PLoS One. 2012;7(1):e29319. (PMID: 22235284) Autoimmun Rev. 2010 Nov;10(1):38-42. (PMID: 20817127) Lupus Sci Med. 2021 Nov;8(1):. (PMID: 34819388) Nat Methods. 2012 Jul;9(7):671-5. (PMID: 22930834) Cells. 2019 May 17;8(5):. (PMID: 31108880) Nat Rev Rheumatol. 2016 Nov 22;12(12):716-730. (PMID: 27872476) Ann Rheum Dis. 2019 Mar;78(3):365-371. (PMID: 30626657) Lupus Sci Med. 2018 Nov 22;5(1):e000286. (PMID: 30538817) N Engl J Med. 2011 Dec 1;365(22):2110-21. (PMID: 22129255) Int J Mol Sci. 2021 Apr 08;22(8):. (PMID: 33917744) Rheumatology (Oxford). 2014 Apr;53(4):583-5. (PMID: 24446470) Drugs. 2021 Oct;81(15):1795-1802. (PMID: 34554438) Ann Rheum Dis. 2013 May;72(5):776-80. (PMID: 23434571) Front Med (Lausanne). 2022 Mar 14;9:830998. (PMID: 35372383) Arthritis Rheum. 2001 Oct;44(10):2331-7. (PMID: 11665973) Thromb Res. 2018 Mar;163:105-116. (PMID: 29407621) Front Immunol. 2021 Apr 20;12:676082. (PMID: 33959133) Int J Biochem Cell Biol. 2012 Sep;44(9):1390-7. (PMID: 22687752) Int J Mol Sci. 2020 Dec 15;21(24):. (PMID: 33333969) Atherosclerosis. 2022 Jun;351:29-40. (PMID: 35365353) J Clin Invest. 2018 Apr 2;128(4):1471-1484. (PMID: 29360642) Signal Transduct Target Ther. 2022 Mar 10;7(1):78. (PMID: 35273164) Nat Cell Biol. 2014 Apr;16(4):305-6. (PMID: 24691258) Sci Rep. 2020 Jul 14;10(1):11568. (PMID: 32665552) J Biol Chem. 2011 Mar 11;286(10):8055-8066. (PMID: 21212269) Ann Rheum Dis. 2019 Dec;78(12):1669-1676. (PMID: 31570366) Nat Rev Rheumatol. 2021 Sep;17(9):515-532. (PMID: 34345022) Front Med (Lausanne). 2022 Apr 08;9:849086. (PMID: 35462989) Nat Commun. 2020 Dec 1;11(1):6149. (PMID: 33262343) Semin Immunopathol. 2022 May;44(3):309-324. (PMID: 35355124) J Clin Invest. 2016 Sep 1;126(9):3495-510. (PMID: 27548530) Arthritis Rheumatol. 2021 Mar;73(3):459-471. (PMID: 32909675) Nat Rev Drug Discov. 2017 Sep;16(9):635-661. (PMID: 28529319) Arthritis Rheumatol. 2019 Sep;71(9):1400-1412. (PMID: 31385462) Blood. 2007 Oct 15;110(8):2907-15. (PMID: 17638846) J Infect Dis. 2010 Mar 15;201(6):936-45. (PMID: 20158391) Int J Mol Sci. 2021 Oct 19;22(20):. (PMID: 34681945) Arthritis Rheum. 2005 May;52(5):1491-503. (PMID: 15880830) Arthritis Care Res (Hoboken). 2014 Apr;66(4):608-16. (PMID: 24106157) Ann Rheum Dis. 2010 Jun;69(6):1136-9. (PMID: 19687018) Int J Cardiol. 2016 Jun 1;212:364-8. (PMID: 27057957) Br J Pharmacol. 2021 May;178(10):2041-2059. (PMID: 31999357) Methods Appl Fluoresc. 2020 Oct 06;8(4):040401. (PMID: 33021203) J Clin Invest. 2016 Sep 1;126(9):3511-25. (PMID: 27548529) Arthritis Rheumatol. 2014 Jun;66(6):1583-95. (PMID: 24644022) Atherosclerosis. 2015 Aug;241(2):297-304. (PMID: 26062989) Arthritis Rheumatol. 2021 May;73(5):816-825. (PMID: 33225631) Pharmacol Res. 2019 Aug;146:104292. (PMID: 31167111) Ann Rheum Dis. 2016 Sep;75(9):1615-21. (PMID: 26458737) Redox Biol. 2020 Feb;30:101420. (PMID: 31935648) Nat Rev Rheumatol. 2022 Oct;18(10):575-590. (PMID: 36097207) Arthritis Rheum. 2007 Nov;56(11):3759-69. (PMID: 17968925) J Card Fail. 2021 Jul;27(7):786-795. (PMID: 33872759) |
| 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 |
Full Text Finder | تدمد: | 1664-3224 |
|---|---|
| DOI: | 10.3389/fimmu.2023.1277267 |