Nox-derived ROS are acutely activated in pressure overload pulmonary hypertension: indications for a seminal role for mitochondrial Nox4
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Pulmonary arterial hypertension is a severe progressive disease with marked morbidity and high mortality in which right ventricular (RV) failure is the major cause of death. Thus knowledge of the mechanisms underlying RV failure is an area of active interest. Previous studies suggest a role of NADPH oxidase in cardiomyocyte dysfunction in the left heart. Here we postulate that acute pressure overload induced by pulmonary artery banding (PAB) leads to a Nox4-initiated increase in reactive oxygen species (ROS) in mouse RV that may lead to feed-forward induction of Nox2. To test our hypothesis, ROS production was measured in RV and left ventricle homogenates. The data show that hydrogen peroxide (H 2 O 2), but not superoxide anion (O 2·−), was increased in the early phases (within 6 h) of PAB in RV and that this increase was diminished by catalase and diphenyleneiodonium chloride but not by SOD, N ω-nitro-l-arginin methyl ester, febuxostat, or indomethacin. H 2 O 2 production in RV was not attenuated in Nox2 null mice subjected to 6 h PAB. Moreover, we observed an upregulation of Nox4 mRNA after 1 h of PAB and an increase in mitochondrial Nox4 protein 6 h post-PAB. In contrast, we observed an increase in Nox2 mRNA 1 day post-PAB. Expression of antioxidant enzymes SOD, catalase, and glutathione peroxidase did not change, but catalase activity increased 6 h post-PAB. Taken together, these findings show a role of mitochondria-localized Nox4 in the early phase of PAB and suggest an involvement of this isozyme in early ROS generation possibly contributing to progression of RV dysfunction and failure.
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NOX4 has been reported to be localized within the mitochondrion either constitutively or in specific pathological conditions, although controversial.
“Additionally, although controversial, NOX4 has been reported to be localized within the mitochondrion either constitutively or in specific pathological conditions (152, 306, 540).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [306]
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Dustin, C. M., Cifuentes-Pagano, E., & Pagano, P. J. (2023) · Springer eBooks · doi:10.1007/978-3-031-23752-2_21 · Cited by 5 · see citing works
Self-citationNAD(P)H oxidase isoforms as therapeutic targets for diabetic complications
Gray, S. P., Jha, J. C., Marco, E. D., & Jandeleit-Dahm, K. A. M. (2014) · Expert Review of Endocrinology & Metabolism · doi:10.1586/17446651.2014.887984 · Cited by 5 · see citing works
Okoye, C. N., Chinnappareddy, N., Stevens, D., & Kamunde, C. (2021) · Comparative Biochemistry and Physiology Part C Toxicology & Pharmacology · doi:10.1016/j.cbpc.2021.109227 · Cited by 4 · see citing works
Davis, E. M., Baust, J., O’Donnell, B. J., Shah, F. A., McDowell, A. L., Guo, L., & O'Donnell, C. P. (2018) · PLoS ONE · doi:10.1371/journal.pone.0208540 · Cited by 2 · see citing works
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How Vascular Smooth Muscle Cells Face The Oxidative Stress In The Pulmonary Arterial Hypertension?
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Molecular Mechanism of Stress Regulation in Cardiac Dysfunction and Hematopathologies
Ali, T. (2015) · HEC National Digital Library
Nejatbakhsh, A. (2016) · YorkSpace (York University)
- Authors
- Frazziano, G., Al Ghouleh, I., Baust, J., Shiva, S., Champion, H. C., & Pagano, P. J.
- Affiliations
- University of Pittsburgh (US)
- Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania;
- Corresponding author
- Pagano, Patrick J.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2014-01-15
- Volume
- 306
- Issue
- 2
- Pages
- H197-H205
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- PMC
- PMC3920131
- OpenAlex
- W1981930504
- Cited by
- 51
- References
- 43
- Citations by year
- 2024: 1 · 2023: 3 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 9 · 2018: 8 · 2017: 6 · 2016: 7 · 2015: 5 · 2014: 3
- FWCI
- 4.06
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL079207, P01HL103455, R01HL112914)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- pulmonary arterial hypertension, pressure overload, NADPH oxidase, NOX4, NOX2, reactive oxygen species, hydrogen peroxide, right heart failure, pulmonary artery banding, antioxidant enzymes, cardiomyocyte dysfunction
- MeSH terms
- NADPH Oxidase 2, NADPH Oxidase 4, Animals, Catalase, Glutathione Peroxidase, Heart Ventricles, Hypertension, Pulmonary, Male, Membrane Glycoproteins, Mice, Inbred C57BL, Mitochondria, RNA, Messenger, Superoxide Dismutase, Up-Regulation, Reactive Oxygen Species, Ventricular Dysfunction, NADPH Oxidases, Mice
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