دورية أكاديمية
أعرض في EDS

Trichostatin A, a histone deacetylase inhibitor suppresses NADPH Oxidase 4-Derived Redox Signalling and Angiogenesis.

التفاصيل البيبلوغرافية
العنوان: Trichostatin A, a histone deacetylase inhibitor suppresses NADPH Oxidase 4-Derived Redox Signalling and Angiogenesis.
المؤلفون: Hakami NY; Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia.; Ophthalmology, University of Melbourne, Department of Surgery, East Melbourne, VIC, Australia.; Department of Pharmacology and Therapeutics, University of Melbourne, Melbourne, VIC, Australia.; Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia., Dusting GJ; Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia.; Ophthalmology, University of Melbourne, Department of Surgery, East Melbourne, VIC, Australia., Peshavariya HM; Centre for Eye Research Australia, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia. hitesh.peshavariya@unimelb.edu.au.; Ophthalmology, University of Melbourne, Department of Surgery, East Melbourne, VIC, Australia. hitesh.peshavariya@unimelb.edu.au.
المصدر: Journal of cellular and molecular medicine [J Cell Mol Med] 2016 Oct; Vol. 20 (10), pp. 1932-44. Date of Electronic Publication: 2016 Jun 14.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
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: Histone Deacetylase Inhibitors/*pharmacology , Hydroxamic Acids/*pharmacology , NADPH Oxidases/*antagonists & inhibitors , Neovascularization, Physiologic/*drug effects , Signal Transduction/*drug effects, Animals ; Capillaries/drug effects ; Capillaries/metabolism ; Cell Movement/drug effects ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Mice ; Models, Biological ; NADPH Oxidase 4 ; NADPH Oxidases/metabolism ; Oxidation-Reduction/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis/drug effects ; Transforming Growth Factor beta1/pharmacology ; Ubiquitination/drug effects ; p300-CBP Transcription Factors/metabolism
مستخلص: Histone deacetylase (HDAC) inhibitors are known to suppress abnormal development of blood vessels. Angiogenic activity in endothelial cells depends upon NADPH oxidase 4 (Nox4)-dependent redox signalling. We set out to study whether the HDAC inhibitor trichostatin A (TSA) affects Nox4 expression and angiogenesis. Nox4 expression was measured by real time PCR and Western blot analysis in endothelial cells. Hydrogen peroxide (H2 O2 ) was measured by amplex(®) red assay in endothelial cells. Nox4 was knocked down by Nox4 shRNA. In vitro angiogenic activities such migration and tubulogenesis were assessed using wound healing and Matrigel assays, respectively. In vivo angiogenic activity was assessed using subcutaneous sponge assay in C57Bl/6 and Nox4-deficient mice. Trichostatin A reduced Nox4 expression in a time- and concentration-dependent manner. Both TSA and Nox4 silencing decreased Nox4 protein and H2 O2 . Mechanistically, TSA reduced expression of Nox4 via ubiquitination of p300- histone acetyltransferase (p300-HAT). Thus, blocking of the ubiquitination pathway using an inhibitor of ubiquitin-activating enzyme E1 (PYR-41) prevented TSA inhibition of Nox4 expression. Trichostatin A also reduced migration and tube formation, and these effects were not observed in Nox4-deficient endothelial cells. Finally, transforming growth factor beta1 (TGFβ1) enhanced angiogenesis in sponge model in C57BL/6 mice. This response to TGFβ1 was substantially reduced in Nox4-deficient mice. Similarly intraperitoneal infusion of TSA (1 mg/kg) also suppressed TGFβ1-induced angiogenesis in C57BL/6 mice. Trichostatin A reduces Nox4 expression and angiogenesis via inhibition of the p300-HAT-dependent pathway. This mechanism might be exploited to prevent aberrant angiogenesis in diabetic retinopathy, complicated vascular tumours and malformations.
(© 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)
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فهرسة مساهمة: Keywords: Nox4; TGFβ1; histone acetyltransferases; histone deacetylase inhibitor; trichostatin A
المشرفين على المادة: 0 (Histone Deacetylase Inhibitors)
0 (Hydroxamic Acids)
0 (Transforming Growth Factor beta1)
3X2S926L3Z (trichostatin A)
BBX060AN9V (Hydrogen Peroxide)
EC 1.6.3.- (NADPH Oxidase 4)
EC 1.6.3.- (NADPH Oxidases)
EC 1.6.3.- (NOX4 protein, human)
EC 2.3.1.48 (p300-CBP Transcription Factors)
EC 2.3.1.48 (p300-CBP-associated factor)
EC 3.4.25.1 (Proteasome Endopeptidase Complex)
تواريخ الأحداث: Date Created: 20160615 Date Completed: 20170711 Latest Revision: 20181113
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC5020625
DOI: 10.1111/jcmm.12885
PMID: 27297729
قاعدة البيانات: MEDLINE
الوصف
تدمد:1582-4934
DOI:10.1111/jcmm.12885