2013
DOI: 10.1089/ars.2012.4666
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NADPH Oxidase-Mediated Triggering of Inflammasome Activation in Mouse Podocytes and Glomeruli During Hyperhomocysteinemia

Abstract: Aim: Our previous studies have shown that NOD-like receptor protein (NALP3) inflammasome activation is importantly involved in podocyte dysfunction and glomerular sclerosis induced by hyperhomocysteinemia (hHcys). The present study was designed to test whether nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-mediated redox signaling contributes to homocysteine (Hcys)-induced activation of NALP3 inflammasomes, an intracellular inflammatory machinery in podocytes in vitro and in vivo. Results: In vitr… Show more

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Cited by 130 publications
(148 citation statements)
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“…These data strongly suggest that NOX2 inhibition during neonatal sepsis attenuates lung inflammation, tissue damage, and alveolar remodeling. Although the use of gp91phox ds-tat in an animal model of sepsis is new, these data are consistent with other reports that indicate NOX2-mediated injury in hypertension, diabetes, and inflammasome activation is inhibited with gp91phox ds-tat (31,54,55). We used gp91phox ds-tat before intraperitoneal LPS injection to generate proof-of-principle data as a potential therapeutic agent in sepsis.…”
Section: Original Researchsupporting
confidence: 82%
“…These data strongly suggest that NOX2 inhibition during neonatal sepsis attenuates lung inflammation, tissue damage, and alveolar remodeling. Although the use of gp91phox ds-tat in an animal model of sepsis is new, these data are consistent with other reports that indicate NOX2-mediated injury in hypertension, diabetes, and inflammasome activation is inhibited with gp91phox ds-tat (31,54,55). We used gp91phox ds-tat before intraperitoneal LPS injection to generate proof-of-principle data as a potential therapeutic agent in sepsis.…”
Section: Original Researchsupporting
confidence: 82%
“…Similar results were obtained with cells from patients with CGD carrying mutations in the CYBB (the NOX2 gene) or with macrophages from gp91phox −/− (44,54). A recent study, however, demonstrated the requirement of NOX2 for activation of NLRP3 by homocysteine in podocytes, both in vitro and in vivo, contributing to kidney inflammation and tissue damage (55). Inhibition of NADPH oxidase activity by apocynin and the genetic deficiency of gp91phox −/− on primary BMMs abrogated the activation of inflammasome by heme.…”
Section: Discussionmentioning
confidence: 97%
“…Dosing of gp91ds-tat was based on reported therapeutic effects in mice. 21 The ds-tat scrambled-and gp91ds-tat-treated CCI mice were anesthetized (100 mg/kg sodium pentobarbital, i.p.) at 7 d post-injury and transcardially perfused with ice-cold 0.9% saline (100 mL), followed by 300 mL of 4% paraformaldehyde.…”
Section: Studymentioning
confidence: 99%