Does NADPH oxidase deficiency cause artery dilatation in humans?

Lorenzo Loffredo, Roberto Carnevale, Valerio Sanguigni, Alessandro Plebani, Paolo Rossi, Claudio Pignata, Domenico De Mattia, Andrea Finocchi, Baldassarre Martire, Maria Cristina Pietrogrande, Silvana Martino, Eleonora Gambineri, Giuliana Giardino, Anna Rosa Soresina, Francesco Martino, Pasquale Pignatelli, Francesco Violi

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

NADPH oxidase is known to modulate the arterial tone, but the role of its specific subunits is still unclear. The objective of this study was to compare the role of p47 and gp91phox (NOX2) on artery dilatation. We conducted a multicenter study enrolling 30 patients with chronic granulomatous disease (CGD) (25 with NOX2 deficiency and 5 with p47phox deficiency) and 30 healthy subjects (HS), matched for gender and age, in whom flow-mediated dilation (FMD), serum activity of NOX2 (soluble NOX2-derived peptide [sNOX2-dp]), urinary isoprostanes (8-iso-PGF2α), and platelet production of isoprostanes and NOX2 were determined. Compared to HS, patients with CGD had significantly higher FMD and lower sNOX2-dp and 8-iso-PGF2α levels. Compared to patients with NOX2 deficiency and HS, patients with p47 phox hereditary deficiency had intermediate FMD and oxidative stress, that is, higher and lower FMD and lower and higher isoprostanes compared to HS and patients with NOX2 deficiency, respectively. In agreement with this finding, an ex vivo study showed higher inhibition of NOX2 activity and lower isoprostane formation in platelets from patients with NOX2 deficiency compared to platelets from ones with p47phox deficiency. Our observations lead to the hypothesis that oxidants are implicated in artery vasoconstriction. Antioxid. Redox Signal. 18, 1491-1496.

Original languageEnglish
Pages (from-to)1491-1496
Number of pages6
JournalAntioxidants and Redox Signaling
Volume18
Issue number12
DOIs
Publication statusPublished - Apr 20 2013

Fingerprint

Isoprostanes
NADPH Oxidase
Platelets
Dilatation
8-epi-prostaglandin F2alpha
Dinoprost
Arteries
Healthy Volunteers
Chronic Granulomatous Disease
Peptides
Oxidative stress
Blood Platelets
Oxidants
Vasoconstriction
Multicenter Studies
Oxidation-Reduction
Oxidative Stress
Serum

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology
  • Physiology
  • Clinical Biochemistry

Cite this

Loffredo, L., Carnevale, R., Sanguigni, V., Plebani, A., Rossi, P., Pignata, C., ... Violi, F. (2013). Does NADPH oxidase deficiency cause artery dilatation in humans? Antioxidants and Redox Signaling, 18(12), 1491-1496. https://doi.org/10.1089/ars.2012.4987

Does NADPH oxidase deficiency cause artery dilatation in humans? / Loffredo, Lorenzo; Carnevale, Roberto; Sanguigni, Valerio; Plebani, Alessandro; Rossi, Paolo; Pignata, Claudio; De Mattia, Domenico; Finocchi, Andrea; Martire, Baldassarre; Pietrogrande, Maria Cristina; Martino, Silvana; Gambineri, Eleonora; Giardino, Giuliana; Soresina, Anna Rosa; Martino, Francesco; Pignatelli, Pasquale; Violi, Francesco.

In: Antioxidants and Redox Signaling, Vol. 18, No. 12, 20.04.2013, p. 1491-1496.

Research output: Contribution to journalArticle

Loffredo, L, Carnevale, R, Sanguigni, V, Plebani, A, Rossi, P, Pignata, C, De Mattia, D, Finocchi, A, Martire, B, Pietrogrande, MC, Martino, S, Gambineri, E, Giardino, G, Soresina, AR, Martino, F, Pignatelli, P & Violi, F 2013, 'Does NADPH oxidase deficiency cause artery dilatation in humans?', Antioxidants and Redox Signaling, vol. 18, no. 12, pp. 1491-1496. https://doi.org/10.1089/ars.2012.4987
Loffredo L, Carnevale R, Sanguigni V, Plebani A, Rossi P, Pignata C et al. Does NADPH oxidase deficiency cause artery dilatation in humans? Antioxidants and Redox Signaling. 2013 Apr 20;18(12):1491-1496. https://doi.org/10.1089/ars.2012.4987
Loffredo, Lorenzo ; Carnevale, Roberto ; Sanguigni, Valerio ; Plebani, Alessandro ; Rossi, Paolo ; Pignata, Claudio ; De Mattia, Domenico ; Finocchi, Andrea ; Martire, Baldassarre ; Pietrogrande, Maria Cristina ; Martino, Silvana ; Gambineri, Eleonora ; Giardino, Giuliana ; Soresina, Anna Rosa ; Martino, Francesco ; Pignatelli, Pasquale ; Violi, Francesco. / Does NADPH oxidase deficiency cause artery dilatation in humans?. In: Antioxidants and Redox Signaling. 2013 ; Vol. 18, No. 12. pp. 1491-1496.
@article{80a764a0776643b8b219f2b468865b33,
title = "Does NADPH oxidase deficiency cause artery dilatation in humans?",
abstract = "NADPH oxidase is known to modulate the arterial tone, but the role of its specific subunits is still unclear. The objective of this study was to compare the role of p47 and gp91phox (NOX2) on artery dilatation. We conducted a multicenter study enrolling 30 patients with chronic granulomatous disease (CGD) (25 with NOX2 deficiency and 5 with p47phox deficiency) and 30 healthy subjects (HS), matched for gender and age, in whom flow-mediated dilation (FMD), serum activity of NOX2 (soluble NOX2-derived peptide [sNOX2-dp]), urinary isoprostanes (8-iso-PGF2α), and platelet production of isoprostanes and NOX2 were determined. Compared to HS, patients with CGD had significantly higher FMD and lower sNOX2-dp and 8-iso-PGF2α levels. Compared to patients with NOX2 deficiency and HS, patients with p47 phox hereditary deficiency had intermediate FMD and oxidative stress, that is, higher and lower FMD and lower and higher isoprostanes compared to HS and patients with NOX2 deficiency, respectively. In agreement with this finding, an ex vivo study showed higher inhibition of NOX2 activity and lower isoprostane formation in platelets from patients with NOX2 deficiency compared to platelets from ones with p47phox deficiency. Our observations lead to the hypothesis that oxidants are implicated in artery vasoconstriction. Antioxid. Redox Signal. 18, 1491-1496.",
author = "Lorenzo Loffredo and Roberto Carnevale and Valerio Sanguigni and Alessandro Plebani and Paolo Rossi and Claudio Pignata and {De Mattia}, Domenico and Andrea Finocchi and Baldassarre Martire and Pietrogrande, {Maria Cristina} and Silvana Martino and Eleonora Gambineri and Giuliana Giardino and Soresina, {Anna Rosa} and Francesco Martino and Pasquale Pignatelli and Francesco Violi",
year = "2013",
month = "4",
day = "20",
doi = "10.1089/ars.2012.4987",
language = "English",
volume = "18",
pages = "1491--1496",
journal = "Antioxidants and Redox Signaling",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "12",

}

TY - JOUR

T1 - Does NADPH oxidase deficiency cause artery dilatation in humans?

AU - Loffredo, Lorenzo

AU - Carnevale, Roberto

AU - Sanguigni, Valerio

AU - Plebani, Alessandro

AU - Rossi, Paolo

AU - Pignata, Claudio

AU - De Mattia, Domenico

AU - Finocchi, Andrea

AU - Martire, Baldassarre

AU - Pietrogrande, Maria Cristina

AU - Martino, Silvana

AU - Gambineri, Eleonora

AU - Giardino, Giuliana

AU - Soresina, Anna Rosa

AU - Martino, Francesco

AU - Pignatelli, Pasquale

AU - Violi, Francesco

PY - 2013/4/20

Y1 - 2013/4/20

N2 - NADPH oxidase is known to modulate the arterial tone, but the role of its specific subunits is still unclear. The objective of this study was to compare the role of p47 and gp91phox (NOX2) on artery dilatation. We conducted a multicenter study enrolling 30 patients with chronic granulomatous disease (CGD) (25 with NOX2 deficiency and 5 with p47phox deficiency) and 30 healthy subjects (HS), matched for gender and age, in whom flow-mediated dilation (FMD), serum activity of NOX2 (soluble NOX2-derived peptide [sNOX2-dp]), urinary isoprostanes (8-iso-PGF2α), and platelet production of isoprostanes and NOX2 were determined. Compared to HS, patients with CGD had significantly higher FMD and lower sNOX2-dp and 8-iso-PGF2α levels. Compared to patients with NOX2 deficiency and HS, patients with p47 phox hereditary deficiency had intermediate FMD and oxidative stress, that is, higher and lower FMD and lower and higher isoprostanes compared to HS and patients with NOX2 deficiency, respectively. In agreement with this finding, an ex vivo study showed higher inhibition of NOX2 activity and lower isoprostane formation in platelets from patients with NOX2 deficiency compared to platelets from ones with p47phox deficiency. Our observations lead to the hypothesis that oxidants are implicated in artery vasoconstriction. Antioxid. Redox Signal. 18, 1491-1496.

AB - NADPH oxidase is known to modulate the arterial tone, but the role of its specific subunits is still unclear. The objective of this study was to compare the role of p47 and gp91phox (NOX2) on artery dilatation. We conducted a multicenter study enrolling 30 patients with chronic granulomatous disease (CGD) (25 with NOX2 deficiency and 5 with p47phox deficiency) and 30 healthy subjects (HS), matched for gender and age, in whom flow-mediated dilation (FMD), serum activity of NOX2 (soluble NOX2-derived peptide [sNOX2-dp]), urinary isoprostanes (8-iso-PGF2α), and platelet production of isoprostanes and NOX2 were determined. Compared to HS, patients with CGD had significantly higher FMD and lower sNOX2-dp and 8-iso-PGF2α levels. Compared to patients with NOX2 deficiency and HS, patients with p47 phox hereditary deficiency had intermediate FMD and oxidative stress, that is, higher and lower FMD and lower and higher isoprostanes compared to HS and patients with NOX2 deficiency, respectively. In agreement with this finding, an ex vivo study showed higher inhibition of NOX2 activity and lower isoprostane formation in platelets from patients with NOX2 deficiency compared to platelets from ones with p47phox deficiency. Our observations lead to the hypothesis that oxidants are implicated in artery vasoconstriction. Antioxid. Redox Signal. 18, 1491-1496.

UR - http://www.scopus.com/inward/record.url?scp=84875143983&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84875143983&partnerID=8YFLogxK

U2 - 10.1089/ars.2012.4987

DO - 10.1089/ars.2012.4987

M3 - Article

VL - 18

SP - 1491

EP - 1496

JO - Antioxidants and Redox Signaling

JF - Antioxidants and Redox Signaling

SN - 1523-0864

IS - 12

ER -