Journal article

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

Nora Y Hakami, Gregory J Dusting, Hitesh M Peshavariya

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE | WILEY | Published : 2016

Abstract

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 asses..

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Grants

Awarded by National Heart Foundation of Australia


Awarded by National Health and Medical Research Council Research Fellowship


Funding Acknowledgements

This study was supported by the National Heart Foundation of Australia Grant-in-Aid (G 12M 6726) and Postdoctoral Fellowship (HMP; PF 11M 6093). GJD is the recipient of a National Health and Medical Research Council Research Fellowship (#1003113). NYH was supported by King Abdulaziz University, Jeddah, SA. The Centre for Eye Research Australia receives Operational Infrastructure Support from the Victorian Government. Adv-Nox4i was a kind gift from Prof John F Keaney Jr, University of Massachusetts Medical School.