دورية أكاديمية
أعرض في EDS

Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation.

التفاصيل البيبلوغرافية
العنوان: Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation.
المؤلفون: Emrich F; Department of Cardiothoracic Surgery, Stanford University, Stanford, California.; Department of Cardiothoracic Surgery, Leipzig University Heart Center, Leipzig, Germany., Penov K; Department of Cardiothoracic Surgery, Stanford University, Stanford, California.; Department of Cardiothoracic Surgery, Leipzig University Heart Center, Leipzig, Germany., Arakawa M; Department of Cardiothoracic Surgery, Stanford University, Stanford, California.; Department of Cardiovascular Surgery, Jichi Medical University, Saitama, Japan., Dhablania N; Department of Cardiothoracic Surgery, Stanford University, Stanford, California., Burdon G; Department of Cardiothoracic Surgery, Stanford University, Stanford, California., Pedroza AJ; Department of Cardiothoracic Surgery, Stanford University, Stanford, California., Koyano TK; Department of Cardiothoracic Surgery, Stanford University, Stanford, California., Kim YM; Department of Cardiovascular Medicine, Stanford University, Stanford, California., Raaz U; Department of Cardiovascular Medicine, Stanford University, Stanford, California., Connolly AJ; Department of Pathology, Stanford University, Stanford, California., Iosef C; Department of Cardiothoracic Surgery, Stanford University, Stanford, California., Fischbein MP; Department of Cardiothoracic Surgery, Stanford University, Stanford, California.
المصدر: Journal of cellular and molecular medicine [J Cell Mol Med] 2019 Oct; Vol. 23 (10), pp. 7000-7009. Date of Electronic Publication: 2019 Aug 11.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101083777 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1582-4934 (Electronic) Linking ISSN: 15821838 NLM ISO Abbreviation: J Cell Mol Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford, England : Wiley-Blackwell
Original Publication: Bucharest : "Carol Davila" University Press, 2000-
مواضيع طبية MeSH: Aneurysm/*complications , Aneurysm/*metabolism , Marfan Syndrome/*complications , Marfan Syndrome/*metabolism , Reactive Oxygen Species/*metabolism, Acetophenones/pharmacology ; Angiotensin II ; Animals ; Aorta/metabolism ; Aorta/pathology ; Disease Models, Animal ; Fibrillin-1/deficiency ; Fibrillin-1/metabolism ; Mice, Inbred C57BL ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; NADPH Oxidases/metabolism
مستخلص: Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS Fbn1 C1039G/+ mouse root/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin-enhanced chemiluminescence (LGCL), Verhoeff's elastin-Van Gieson staining (elastin breakdown) and in situ zymography for protease activity. Fbn1 C1039G/+ AS- or DES-derived smooth muscle cells (SMC) were treated with anti-TGF-β antibody, angiotensin II (AngII), anti-TGF-β antibody + AngII, or isotype control. ROS were detected during early aneurysm formation in the Fbn1 C1039G/+ AS aorta, but absent in normal-sized DES aorta. Fbn1 C1039G/+ mice treated with the unspecific NADPH oxidase inhibitor, apocynin reduced AS aneurysm formation, with attenuated elastin fragmentation. In situ zymography revealed apocynin treatment decreased protease activity. In vitro SMC studies showed Fbn1 C1039G/+ -derived AS SMC had increased NADPH activity compared to DES-derived SMC. AS SMC NADPH activity increased with AngII treatment and appeared TGF-β dependent. In conclusion, ROS play a role in MFS aneurysm development and correspond anatomically with aneurysmal aortic segments. ROS inhibition via apocynin treatment attenuates MFS aneurysm progression. AngII enhances ROS production in MFS AS SMCs and is likely TGF-β dependent.
(© 2019 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)
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معلومات مُعتمدة: R01 AR066629 United States AR NIAMS NIH HHS
فهرسة مساهمة: Keywords: Marfan syndrome; aneurysm; reactive oxygen species
المشرفين على المادة: 0 (Acetophenones)
0 (Fibrillin-1)
0 (Reactive Oxygen Species)
11128-99-7 (Angiotensin II)
B6J7B9UDTR (acetovanillone)
EC 1.6.3.- (NADPH Oxidases)
تواريخ الأحداث: Date Created: 20190813 Date Completed: 20200902 Latest Revision: 20210110
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6787454
DOI: 10.1111/jcmm.14587
PMID: 31402541
قاعدة البيانات: MEDLINE
الوصف
تدمد:1582-4934
DOI:10.1111/jcmm.14587