دورية أكاديمية

Causes and Consequences of miR-150-5p Dysregulation in Myasthenia Gravis.

التفاصيل البيبلوغرافية
العنوان: Causes and Consequences of miR-150-5p Dysregulation in Myasthenia Gravis.
المؤلفون: Cron MA; Center of Research in Myology, Sorbonne University, INSERM, Association Institute of Myology - UMRS 974, Paris, France., Maillard S; Center of Research in Myology, Sorbonne University, INSERM, Association Institute of Myology - UMRS 974, Paris, France., Truffault F; Center of Research in Myology, Sorbonne University, INSERM, Association Institute of Myology - UMRS 974, Paris, France., Gualeni AV; Department of Pathology and Laboratory Medicine, Istituto Nazionale dei Tumori, Milan, Italy., Gloghini A; Department of Pathology and Laboratory Medicine, Istituto Nazionale dei Tumori, Milan, Italy., Fadel E; Marie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France., Guihaire J; Marie Lannelongue Hospital, Paris-Sud University, Le Plessis-Robinson, France., Behin A; Neuromuscular Disease Center, AIM, Pitié-Salpêtrière Hospital, AP-HP, Paris, France., Berrih-Aknin S; Center of Research in Myology, Sorbonne University, INSERM, Association Institute of Myology - UMRS 974, Paris, France., Le Panse R; Center of Research in Myology, Sorbonne University, INSERM, Association Institute of Myology - UMRS 974, Paris, France.
المصدر: Frontiers in immunology [Front Immunol] 2019 Mar 29; Vol. 10, pp. 539. Date of Electronic Publication: 2019 Mar 29 (Print Publication: 2019).
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: B-Lymphocytes/*immunology , CD4-Positive T-Lymphocytes/*immunology , CD8-Positive T-Lymphocytes/*immunology , MicroRNAs/*immunology , Myasthenia Gravis/*immunology, Adolescent ; Adult ; Female ; Germinal Center/immunology ; Germinal Center/pathology ; Humans ; Male ; Myasthenia Gravis/pathology ; Proto-Oncogene Mas ; Proto-Oncogene Proteins c-myb/immunology ; Receptors, Nicotinic/immunology ; Thymus Gland/immunology ; Thymus Gland/pathology
مستخلص: Autoimmune Myasthenia gravis (MG) is a chronic neuromuscular disease mainly due to antibodies against the acetylcholine receptor (AChR) at the neuromuscular junction that induce invalidating muscle weaknesses. In early-onset MG, the thymus is the effector organ and is often characterized by B-cell infiltrations leading to ectopic germinal center (GC) development. The microRNA miR-150-5p has been previously characterized as a biomarker in MG due to its increase in the serum of patients and its decrease after thymectomy, correlated with an improvement of symptoms. Here, we investigated the causes and consequences of the miR-150 increase in the serum of early-onset MG patients. We observed that miR-150 expression was upregulated in MG thymuses in correlation with the presence of thymic B cells and showed by in situ hybridization experiments, that miR-150 was mainly expressed by cells of the mantle zone of GCs. However, we did not observe any correlation between the degree of thymic hyperplasia and the serum levels in MG patients. In parallel, we also investigated the expression of miR-150 in peripheral blood mononuclear cells (PBMCs) from MG patients. We observed that miR-150 was down-regulated, especially in CD4 + T cells compared to controls. These results suggest that the increased serum levels of miR-150 could result from a release from activated peripheral CD4 + T cells. Next, we demonstrated that the in vitro treatment of PBMCs with miR-150 or antimiR-150 oligonucleotides, respectively, decreased or increased the expression of one of its major target gene: the proto-oncogene MYB , a well-known actor of hematopoiesis. These results revealed that increased serum levels of miR-150 in MG patients could have a functional effect on PBMCs. We also showed that antimiR-150 caused increased cellular death of CD4 + and CD8 + T cells, along with the overexpression of pro-apoptotic genes targeted by miR-150 suggesting that miR-150 controlled the survival of these cells. Altogether, these results showed that miR-150 could play a role in MG both at the thymic level and in periphery by modulating the expression of target genes and peripheral cell survival.
References: Scand J Immunol. 2004 Apr;59(4):408-14. (PMID: 15049785)
Nat Immunol. 2004 Jul;5(7):721-9. (PMID: 15195090)
Blood. 2006 Jul 15;108(2):432-40. (PMID: 16543475)
Proc Natl Acad Sci U S A. 2007 Apr 24;104(17):7080-5. (PMID: 17438277)
Nat Med. 2007 Oct;13(10):1241-7. (PMID: 17906637)
Cell. 2007 Oct 5;131(1):146-59. (PMID: 17923094)
Semin Immunol. 2008 Aug;20(4):247-56. (PMID: 18585056)
Lab Invest. 2009 Jun;89(6):708-16. (PMID: 19349957)
Ann Neurol. 2009 Oct;66(4):521-31. (PMID: 19847900)
Arthritis Res Ther. 2010;12(3):R81. (PMID: 20459811)
Cell Mol Immunol. 2010 Nov;7(6):447-53. (PMID: 20852654)
Arthritis Rheum. 2011 Feb;63(2):535-44. (PMID: 21280008)
Proc Natl Acad Sci U S A. 2011 Mar 22;108(12):5003-8. (PMID: 21383194)
Cell Mol Immunol. 2011 Sep;8(5):380-7. (PMID: 21822298)
Gut. 2012 Oct;61(10):1447-53. (PMID: 22052060)
PLoS One. 2011;6(11):e27580. (PMID: 22110677)
Immunobiology. 2013 Mar;218(3):373-81. (PMID: 22704519)
BMC Genomics. 2012 Aug 01;13:357. (PMID: 22849433)
Clin Exp Immunol. 2013 Jan;171(1):91-9. (PMID: 23199328)
Ann Neurol. 2013 Jun;73(6):729-40. (PMID: 23494648)
J Am Soc Nephrol. 2013 Jun;24(7):1073-87. (PMID: 23723424)
PLoS One. 2013 Sep 26;8(9):e75348. (PMID: 24205408)
Front Immunol. 2014 Feb 10;5:43. (PMID: 24575093)
Exp Mol Pathol. 2014 Jun;96(3):422-5. (PMID: 24768587)
PLoS One. 2014 May 14;9(5):e95920. (PMID: 24828336)
Immunology. 2015 Jan;144(1):1-10. (PMID: 25093579)
Ann Clin Transl Neurol. 2014 Jan;1(1):49-58. (PMID: 25356381)
PLoS One. 2014 Dec 04;9(12):e113842. (PMID: 25474406)
Oncol Rep. 2015 Feb;33(2):819-25. (PMID: 25482320)
Mol Med. 2015 Jan 09;21:123-33. (PMID: 25584781)
J Clin Pathol. 2015 Aug;68(8):661-4. (PMID: 25934842)
Sci Rep. 2015 Nov 09;5:16399. (PMID: 26549197)
Sci Transl Med. 2015 Nov 11;7(313):313ra178. (PMID: 26560356)
J Immunol. 2016 Feb 15;196(4):1636-45. (PMID: 26746193)
J Clin Invest. 2016 Apr 1;126(4):1525-37. (PMID: 26999605)
Clin Lab. 2016;62(4):631-8. (PMID: 27215082)
Clin Rev Allergy Immunol. 2017 Feb;52(1):108-124. (PMID: 27273086)
N Engl J Med. 2016 Aug 11;375(6):511-22. (PMID: 27509100)
Front Immunol. 2016 Oct 17;7:430. (PMID: 27799933)
N Engl J Med. 2016 Dec 29;375(26):2570-2581. (PMID: 28029925)
Immunity. 2017 Jan 17;46(1):78-91. (PMID: 28099866)
RNA Biol. 2017 Nov 2;14(11):1534-1543. (PMID: 28277980)
PLoS One. 2017 Mar 24;12(3):e0174585. (PMID: 28339495)
Cell Rep. 2017 Sep 12;20(11):2584-2597. (PMID: 28903040)
Ann N Y Acad Sci. 2018 Jan;1412(1):137-145. (PMID: 29125185)
PLoS One. 2018 Feb 15;13(2):e0193157. (PMID: 29447268)
Neurol Neuroimmunol Neuroinflamm. 2018 Mar 01;5(3):e450. (PMID: 29511707)
Autoimmun Rev. 2018 Jun;17(6):588-600. (PMID: 29655674)
Gene. 2018 Jul 30;665:6-17. (PMID: 29704633)
J Neuroimmunol. 2018 Aug 15;321:164-170. (PMID: 29804819)
J Neurol Neurosurg Psychiatry. 1985 Dec;48(12):1246-52. (PMID: 4087000)
J Immunol Methods. 1974 Aug;5(3):249-52. (PMID: 4427075)
J Neuroimmunol. 1997 Apr;74(1-2):45-54. (PMID: 9119978)
Ann Neurol. 1997 Jun;41(6):731-41. (PMID: 9189034)
فهرسة مساهمة: Keywords: MYB; antimir-150; autoimmunity; germinal center; microRNA
المشرفين على المادة: 0 (MAS1 protein, human)
0 (MIRN150 microRNA, human)
0 (MYB protein, human)
0 (MicroRNAs)
0 (Proto-Oncogene Mas)
0 (Proto-Oncogene Proteins c-myb)
0 (Receptors, Nicotinic)
تواريخ الأحداث: Date Created: 20190416 Date Completed: 20200804 Latest Revision: 20211204
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6450174
DOI: 10.3389/fimmu.2019.00539
PMID: 30984166
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2019.00539