Overexpression of the Superoxide Anion and NADPH Oxidase Isoforms 1 and 4 (NOX1 and NOX4) in Allergic Nasal Mucosa

Moon, Joon; Kim, Tae Hoon; Lee, Heung Man; Lee, Jun Young; Choe, Whan; Kim, Ha Kyun; Lee, Jung Hoon; Oh, Kyoung Ho; Lee, Sang Hag

doi:10.2500/ajra.2009.23.3340

Cited by 18 publications

(23 citation statements)

References 19 publications

(36 reference statements)

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“…In the meantime, TGF-b1 induces ROS production as part of its signal transduction pathway through the superoxide free radical-producing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase catalytic subunit NOX4 (25). Compared with the control nasal mucosa, the oxidative stress marker malondialdehyde, NOX1, and NOX4 increase, whereas the antioxidant superoxide dismutase and nitric oxide (NO) decrease in CRSwNP tissues (26). A recent GA (2) LEN network research in 19 European centers with postal questionnaires has shown that CRS is more common in smokers than in nonsmokers (OR 1.7: 95% CI 1.6-1.9), suggesting that smoking cessation may be an important therapeutic option for CRS patients (27).…”

Section: Pathways Driving Tgf-b1mentioning

confidence: 99%

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Yang

Zhang

Feng

et al. 2014

Allergy

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Transforming growth factor-beta 1 (TGF-b1) has been reported being involved in the remodeling and immunosuppression processes of inflammatory airway diseases; understanding the regulation of TGF-b1 is therefore a key to unravel the pathomechanisms of these diseases. This review briefly summarizes the current knowledge on the influencing factors for driving TGF-b1 and its regulatory pathways in inflammatory airway diseases and discusses possible therapeutic approaches to TGF-b1 control. The factors include smoking and oxidative stress, prostaglandins (PGs), leukotrienes (LTs), bradykinin (BK), and microRNAs (miRs). Based on the summary, new innovative treatment strategies may be developed for inflammatory airway diseases with an impaired expression of TGF-b1.The transforming growth factor-beta (TGF-b) superfamily is critically involved in embryonic development, organogenesis, and tissue homeostasis. It acts as multifunctional regulators of cell growth and differentiation and consists of more than 40 members, mainly including TGF-bs, bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), activins, and inhibins. Between these superfamily members, there is a complex network of regulatory mechanisms (1, 2).Possessing immunomodulatory and fibrogenic characteristics, TGF-b1 is a pleiotropic and multifunctional cytokine secreted from various types of cells, such as endothelial, epithelial and smooth muscle cells, as well as fibroblasts and most immune system cells.Transforming growth factor-beta 1 regulation is unique because it is targeted to the extracellular matrix as a biologically inactive complex, which consists of a mature 25-kDa polypeptide dimer (TGF-b), a latency-associated protein (LAP), and a latent TGF-b-binding protein (LTBP). Active TGF-b is released from the latent complex that was activated via cleavage by proteases and other molecules. The activated TGF-b then becomes a ligand for TGF-b type I and II receptors, leading to receptor Smad (R-Smad) phosphorylation, which subsequently binds to the common-partner Smad (co-Smad), and becoming Smad complexes. The Smad complexes translocate into the nucleus and combine with several transcription factors, thereby becoming a transcriptional active complex that activates target genes transcription. In Abbreviations AHR, airway hyper-responsiveness; BAMBI, BMP and activin membrane-bound inhibitor; BK, bradykinin; BMP, bone morphogenetic protein; CCL2/MCP-1, chemokine (CC motif) ligand 2/monocyte chemotactic protein-1; COPD, chronic obstructive pulmonary disease; CRS, chronic rhinosinusitis; CysLT, cysteinyl leukotriene; FoxP3, forkhead box P3; LAP, latency-associated protein; LTBP, latent TGF-b-binding protein; miR, microRNA; PG, prostaglandin; RORc, RAR-related orphan receptor C; TGF-b1, transforming growth factor-beta 1.Allergy 69 (2014) 699-707

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Section: Pathways Driving Tgf-b1mentioning

confidence: 99%

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Yang

Zhang

Feng

et al. 2014

Allergy

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“…diseases, other than asthma. Moon et al (16) have shown that the expression of NADPH oxidase (NOX)1 and NOX4, and superoxide anion was increased in the nasal mucosa of patients with allergic rhinitis and nasal polyps compared to healthy individuals. Profita et al (17) reported higher FE NO and IL-5 levels and lower pH in nasal and oral EBC of children with atopic dermatitis, allergic rhinitis, and asthma.…”

Section: Introductionmentioning

confidence: 99%

“…Moon et al. (16) have shown that the expression of NADPH oxidase (NOX)1 and NOX4, and superoxide anion was increased in the nasal mucosa of patients with allergic rhinitis and nasal polyps compared to healthy individuals. Profita et al.…”

mentioning

confidence: 99%

Oxidative stress in the airways of children with asthma and allergic rhinitis

Celik

Tuncer

Soyer

et al. 2012

Pediatric Allergy Immunology

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“…These findings might suggest that IL-17A activity generates the NF-B translocation to the nucleus via MEKK1 signaling cascades, promoting an increase of NF-B at binding sites of genes involved in nasal epithelial cells activation during airway inflammation. NOX-4, localized mainly in the epithelial layer, may play an important role in reactive oxygen species production, contributing to the oxidative stress in allergic rhinitis and nasal polyp tissues [33]. NOX family is a key component of the so-called redox signaling system regulating many cellular responses by intracellular ROS content [34].…”

Section: Discussionmentioning

confidence: 99%

Effect of high, medium, and low molecular weight hyaluronan on inflammation and oxidative stress in an in vitro model of human nasal epithelial cells

Albano¹,

Bonanno²,

Cavalieri

et al. 2016

5.1 Airway Pharmacology and Treatment

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IL-17A is involved in the activation of oxidative stress and inflammation in nasal epithelial cells. Hyaluronan (HA) in its high molecular weight form (HMW-HA) shows anti-inflammatory responses in contrast to low and medium molecular weight HA (LMW-HA and MMW-HA). The aim of this study was to investigate the pro-or anti-inflammatory biologic function of HA at different molecular weight in an in vitro model of nasal inflammation IL-17A mediated. We evaluated the ERK1/2 and I B phosphorylation, NF-B signal pathway activation, ROS production, IL-8 and NOX-4 protein, and mRNA levels, in nasal epithelial cells RPMI 2650 stimulated with recombinant human (rh) IL-17A. Furthermore, the cells were treated with HMW-HA, MMW-HA, LMW-HA, and U0126. Our results showed that rhIL-17A increased the ERK1/2, I B phosphorylation and NF-B signal pathway activation, ROS production, IL-8 and NOX-4 proteins, and mRNA levels. The addiction of HMW-HA or U0126 showed a significant downregulatory effect on inflammation due to the rhIL-17A stimulation in nasal epithelial cells. IL-17A is able to generate oxidative stress and inflammation via the activation of ERK1/2/NF-B pathway in nasal epithelial cells. The HMW-HA might represent a coadjuvant of the classic anti-inflammatory/antioxidative treatment of nasal epithelial cells during IL-17A nasal inflammation.

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Overexpression of the Superoxide Anion and NADPH Oxidase Isoforms 1 and 4 (NOX1 and NOX4) in Allergic Nasal Mucosa

Abstract: These results indicate that NOX1 and NOX4 may play an important role in reactive oxygen species production, contributing to the oxidative stress in allergic rhinitis and nasal polyp tissues.

Cited by 18 publications

References 19 publications

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Transforming growth factor‐beta 1 pathways in inflammatory airway diseases

Oxidative stress in the airways of children with asthma and allergic rhinitis

Effect of high, medium, and low molecular weight hyaluronan on inflammation and oxidative stress in an in vitro model of human nasal epithelial cells

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