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A gp91phox Containing NADPH Oxidase Selectively Expressed in Endothelial Cells Is a Major Source of Oxygen Radical Generation in the Arterial Wall
Abstract
Abstract —Reactive oxygen species (ROS) play an important role in regulating vascular tone and intracellular signaling; the enzymes producing ROS in the vascular wall are, however, poorly characterized. We investigated whether a functionally active NADPH oxidase similar to the leukocyte enzyme, ie, containing the subunits p22phox and gp91phox, is expressed in endothelial cells (ECs) and smooth muscle cells (SMCs). Phorbol 12-myristate 13-acetate (PMA), a stimulus for leukocyte NADPH oxidase, increased ROS generation in cultured ECs and endothelium-intact rat aortic segments, but not in SMCs or endothelium-denuded arteries. NADPH enhanced chemiluminescence in all preparations. p22phox mRNA and protein was detected in ECs and SMCs, whereas the expression of gp91phox was confined to ECs. Endothelial gp91phox was identical to the leukocyte form as determined by sequence analysis. In contrast, mitogenic oxidase-1 (mox1) was expressed in SMCs, but not in ECs. To determine the functional relevance of gp91phox expression, experiments were performed in aortic segments from wild-type, gp91phox − /− , and endothelial NO synthase (eNOS) − /− mice. PMA-induced ROS generation was comparable in aortae from wild-type and eNOS − /− mice, but was attenuated in segments from gp91phox − /− mice. Endothelium-dependent relaxation was greater in aortae from gp91phox − /− than from wild-type mice. The ROS scavenger tiron increased endothelium-dependent relaxation in segments from wild-type, but not from gp91phox − /− mice. These data demonstrate that ECs, in contrast to SMCs, express a gp91phox-containing leukocyte-type NADPH oxidase. This enzyme is a major source for arterial ROS generation and affects the bioavailability of endothelium-derived NO. ( Circ Res. 2000;87:26-32.)
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“NOX2 expression has been also reported in other cell types including endothelial cells and adventitial fibroblasts (376, 382, 657, 714, 715, 736, 876) (FIGURE 9, Table 5).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [376]
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Self-citationAn NAD(P)H oxidase regulates growth and transcription in melanoma cells
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“In endothelial cells, a functionally active NADPH oxidase closely resembling the leukocyte NADPH oxidase has been described [13,14].”
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Csányi, G., Taylor, W. R., & Pagano, P. J. (2009) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2009.07.022 · Cited by 131
“In contrast, p67phox and Nox2 protein are undetectable in aortic smooth muscle [40,64] (Table 1).”
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“All these data highlight the specific role of NADPH oxidase in augmentation of local tissue oxidative stress (124, 195).”
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“Recently, a gp91phox-containing phagocyte-type NADPH oxidase has been reported in endothelial cells of various vascular beds (2, 12, 13, 21).”
BackgroundNovel Nox inhibitor of oxLDL-induced reactive oxygen species formation in human endothelial cells
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“Although this study does not provide data to support this hypothesis, it is possible that the increased vascular superoxide production mainly originates from a vascular NAD(P)H oxidase (18, 35) and hence isoprostanes F2 could not accurately reflect the increased aortic oxidative stress.”
Oxidative Stress Impairs Endothelial Progenitor Cell Function
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“NADPH oxidase is a major source of ROS in the vasculature (34), with several studies suggesting that gp91phox (also referred to as Nox2) is a critical component of the ROS-generating NADPH oxidase activated by a range of stimulants in ECs (27, 33, 63).”
Oxidative stress and hypertension
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“With regard to physiological responses, Nox-derived ROS have been linked to ECs migration and ischemia-induced angiogenesis [20].”
BackgroundInfluentialRedox signaling in central neural regulation of cardiovascular function
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“Endothelial cells express all the subunits of the phagocyte oxidase, including gp91, but they also contain the Nox-1 and Nox-4 catalytic subunit homologues (Gorlach et al., 2000; Jones et al., 1996; Lassegue et al., 2001).”
InfluentialNADPH oxidase promotes NF-kappaB activation and proliferation in human airway smooth muscle.
Brar, S., Kennedy, T., Sturrock, A., Huecksteadt, T., Quinn, M., Murphy, T. M., Chitano, P., & Hoidal, J. (2002) · American Journal of Physiology - Lung cellular and Molecular Physiology · doi:10.1152/ajplung.00206.2001 · Cited by 118
“In endothelium (22) and adventitial fibroblasts (41), the membrane oxidase components appear identical to the respective - and -subunits, p22phox and gp91phox, present in leukocytes.”
BackgroundInfluentialNO‐mediated regulation of NAD(P)H oxidase by laminar shear stress in human endothelial cells
Duerrschmidt, N., Stielow, C., Müller, G. M., Pagano, P. J., & Morawietz, H. (2006) · The Journal of Physiology · doi:10.1113/jphysiol.2006.111070 · Cited by 116
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Wingler, K., Hermans, J., Schiffers, P., Moens, A., Paul, M., & Schmidt, H. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01249.x · Cited by 113
“Nevertheless, it can be said with some certainty that NOX2 is not only present in leukocytes, but also in endothelial cells (Gorlach et al., 2000; Bedard and Krause, 2007), fibroblasts (Chamseddine and Miller, 2003) and cardiac myocytes (Nabeebaccus et al.”
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“…enzymatic hydroxylation of proline residues within HIF-a subunits constitutes 0 Downloaded from https://academic.oup.com/cardiovascres/article-abstract/71/2/195/275550 by guest on 28 July 2018 Downloaded fr by guest on 28 July 20 the critical modification that determines protein stability.”
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“A rapid posttranslational activation and/or an increased expression of oxidase subunits can be involved in the upregulation of NOX activity (14, 35).”
BackgroundNovel isoforms of NADPH-oxidase in cerebral vascular control
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“On stimulation, several cytosolic regulatory subunits, including p47, p40, p67, and the small G proteins Rac1 or Rac2, are recruited to the plasma membrane to complex with gp91/p22 and induce enzyme activation (4, 22, 30).”
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BackgroundAtheroprotective effects of antioxidants through inhibition of mitogen-activated protein kinases.
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“For the role of NOX-dependent Ang II signaling in the endothelium see NOXs in the endothelium-dependent relaxation.”
BackgroundEndothelial dysfunction and inflammation: What is the link?
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Metadata
- Authors
- Görlach, A., Brandes, R. P., Nguyen, K., Amidi, M., Dehghani, F., & Busse, R.
- Affiliations
- From the Institut für Kardiovaskuläre Physiologie (A.G., R.P.B., K.N., M.A., R.B.), and Institut für Anatomie II (F.D.), Klinikum der J.W. Goethe-Universität, Frankfurt/Main, Germany.
- Goethe University Frankfurt (DE)
- Corresponding author
- Brandes, R. P.
- Venue
- Circulation Research
- Published
- 2000-07-07
- Volume
- 87
- Issue
- 1
- Pages
- 26-32
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- OpenAlex
- W2169235788
- Cited by
- 598
- References
- 28
- Citations by year
- 2026: 3 · 2024: 4 · 2023: 5 · 2022: 14 · 2021: 12 · 2020: 8 · 2019: 11 · 2018: 10 · 2017: 17 · 2016: 23 · 2015: 13 · 2014: 25 · 2013: 18 · 2012: 28
- FWCI
- 26.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutscher Akademischer Austauschdienst
- Deutsche Forschungsgemeinschaft (SFB 553, TP B1)
- Genentech
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- gp91phox, NADPH oxidase, endothelial cells, reactive oxygen species, oxygen free radicals, arterial wall, smooth muscle cells, p22phox, endothelium-dependent relaxation, nitric oxide bioavailability, endothelial nitric oxide synthase, chemiluminescence, Tiron, aorta
- MeSH terms
- NADPH Oxidase 2, Acetylcholine, Animals, Aorta, Endothelium, Vascular, Free Radicals, Membrane Glycoproteins, Muscle, Smooth, Vascular, Nitric Oxide, Tetradecanoylphorbol Acetate, Reactive Oxygen Species, NADPH Oxidases, Reverse Transcriptase Polymerase Chain Reaction, Mice, Rats
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