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 journalArticlepeer-review

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

ASJC Scopus subject areas

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

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