Reactive Nitrogen Species Augment Fibroblast-Mediated Collagen Gel Contraction, Mediator Production, and Chemotaxis

Sugiura, Hiroaki; Liu, Xiangde; Kobayashi, Tetsu; Togo, Shinsaku; Ertl, Ronald F.; Kawasaki, Shin; Kamio, Koichiro; Wang, Xingqi; Mao, Lijun; Shen, Lei; Hogaboam, Cory M.; Rennard, Stephen I.

doi:10.1165/rcmb.2005-0339oc

Cited by 46 publications

(45 citation statements)

References 34 publications

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“…Recently, we have shown that peroxynitrite, one of the RNS, stimulates fibroblasts. Peroxynitrite stimulates the differentiation of fibroblasts into myofibroblasts and extracellular matrix protein production in vitro [23,30], suggesting that RNS induce fibroblast-mediated profibrotic responses. In the current study, free 3-nitrotyrosine caused the inhibition of tissue remodelling in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Collagen gels were prepared as described previously [22,23]. Briefly, RTTC, distilled water and 46 concentrated DMEM were combined so that the final mixture resulted in 0.75 mg?mL -1 collagen, with a physiological ionic strength of 16 DMEM and a pH of 7.4.…”

Section: Collagen Gel Contraction Assaymentioning

confidence: 99%

“…Measurement of fibronectin, TGF-b1 and VEGF by ELISA Fibronectin, TGF-b1 and VEGF in the media of the monolayer culture were determined by ELISA according to a previous report [23].…”

Section: Collagen Gel Contraction Assaymentioning

confidence: 99%

“…Cell migration was assessed using the Boyden blindwell chamber (Neuroprobe Inc., Gaithersburg, MD, USA) as previously described [23,24]. Briefly, 26 mL of serum-free DMEM containing human fibronectin (20 mg?mL -1 ) was placed into the bottom wells.…”

Section: Chemotaxis Assaymentioning

confidence: 99%

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3-Nitrotyrosine inhibits fibroblast-mediated collagen gel contraction and chemotaxis

et al. 2009

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Reactive nitrogen species induce tissue inflammation and nitrate tyrosine residues of various kinds of proteins. Recent studies have established that the free amino acid form of 3-nitrotyrosine induces cytotoxity and growth inhibition and alters the cellular function in cultured cells. The aim of this study was to evaluate whether 3-nitrotyrosine could affect tissue remodelling in fibroblasts. To accomplish this, human fetal lung fibroblasts (HFL-1) were used to assess the fibroblast-mediated contraction of floating gels and chemotaxis towards fibronectin. In addition, the ability of fibroblasts to release fibronectin, transforming growth factor (TGF)-b1, fibronectin and vascular endothelial growth factor (VEGF) was assessed. 3-Nitrotyrosine significantly inhibited gel contraction (p,0.01) compared with control and this inhibition was abolished by nitric oxide synthase (NOS) inhibitor. 3-Nitrotyrosine did not affect TGF-b1 and VEGF but significantly decreased fibronectin release (p,0.01) into the media. 3-Nitrotyrosine significantly inhibited chemotaxis towards fibronectin through suppression of a 5 b 1 integrin expression (p,0.01). NOS inhibitor also reversed 3-nitrotyrosine-inhibited chemotaxis (p,0.01). Finally, 3-nitrotyrosine enhanced the expression of the inducible type of NOS (p,0.01) and nitric oxide release (p,0.01) through nuclear factor-kB activation. These results suggest that the free amino acid form of 3-nitrotyrosine can affect the tissue repair process by modulating nitric oxide production.

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Section: Discussionmentioning

confidence: 99%

Section: Collagen Gel Contraction Assaymentioning

confidence: 99%

“…Measurement of fibronectin, TGF-b1 and VEGF by ELISA Fibronectin, TGF-b1 and VEGF in the media of the monolayer culture were determined by ELISA according to a previous report [23].…”

Section: Collagen Gel Contraction Assaymentioning

confidence: 99%

Section: Chemotaxis Assaymentioning

confidence: 99%

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3-Nitrotyrosine inhibits fibroblast-mediated collagen gel contraction and chemotaxis

et al. 2009

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“…The baseline expression of XOR is low; however, transcription can be up-regulated due to several factors, such as hypoxia, lipopolysaccharide (LPS), IFN-γ, IL-1, IL-6, tumor necrosis factor-α (TNF-α), and steroid stimulation. XOR activation is increased in the late allergic response phase (37).…”

Section: Endogenous Oxidants and Allergic Asthmamentioning

confidence: 99%

Recent developments in the role of reactive oxygen species in allergic asthma

Zhong

et al. 2017

J. Thorac. Dis.

131

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Allergic asthma has a global prevalence, morbidity, and mortality. Many environmental factors, such as pollutants and allergens, are highly relevant to allergic asthma. The most important pathological symptom of allergic asthma is airway inflammation. Accordingly, the unique role of reactive oxygen species It is well known that reactive oxygen species (ROS), endogenous nitric oxide (NO) and NO derived reactive nitrogen species (RNS) have been reported to mediate oxidative stress and airway inflammation and pathogenesis. However, ROS are more common in allergic asthma development (6,7). Hence, in our review, we mainly focus on the relationship between ROS and allergic asthma. ROS, such as hydrogen peroxide, may be directly or indirectly involved in epithelial cell apoptosis and inactivation of antioxidant enzymes and contribute to allergic asthma (8-11). ROS are derived from endogenous or exogenous oxidants. Endogenous ROS are composed of mitochondria, NADPH, and the xanthine/xanthine oxidase (XO) system. Exogenous sources of ROS production have been linked to strong oxidizing gases, such as ozone (O 3 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ) and particulate matter (PM), which are a major component of air pollution (12,13). The oxygen stress level in asthma is increased because of inflammatory cells in vivo, and cigarette smoke (CS) or PM produces ROS in vitro. For example, compared with normal subjects, the level of H 2 O 2 and superoxide that are produced by eosinophils and neutrophils are significantly increased in asthma patients (14). Increased levels of ROS can cause harmful pathophysiological disorders of allergic asthma. Studies have reported that excessive ROS can damage DNA, carbohydrates, proteins, and lipids, ultimately leading to an increased inflammatory response in allergic asthma (15,16). In this review, we will discuss the updated pathophysiological and mechanisms of oxidative stress relating to allergic asthma. Exogenous oxidants and allergic asthmaPatients' exposure to the environmental atmosphere is the main way that exogenous oxidative stress is induced (17). CS is a complex mixture including more than 4,000 different compounds. It has been demonstrated that inhaled CS can increase ROS levels. Most of these compounds have ability to generate ROS during their metabolism. The mechanism of CS induced inflammation is incorporated with oxidative stress leading to cell death and oxidative DNA damage via apoptosis and/or necrosis (7). It was reported that antioxidants have the ability to protect cells from cigarette smoke extract (CSE) induced apoptosis (18). Isolated human airway smooth muscle (hASM) cells were used to determine Ca 2+ responses and hASM proliferation, as well as ROS level and cytokine generation, by incubating these cells in the presence or absence of CSE. The results revealed that Ca 2+ regulatory proteins alter airway remolding and function in smoking-related airway disease, especially allergic asthma (19). CSE can damage bronchial epithelial cells from asthm...

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Cancer‐associated fibroblast migration in non‐small cell lung cancers is modulated by increased integrin α11 expression

et al. 2021

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Cancer-associated fibroblasts (CAFs) regulate cancer progression through the modulation of extracellular matrix (ECM) and cancer cell adhesion. While undergoing a series of phenotypic changes, CAFs control cancer-stroma interactions through integrin receptor signaling. Here, we isolated CAFs from patients with non-small cell lung cancer (NSCLC), and examined their gene expression profiles. We identified collagen type XI α1 (COL11A1), integrin α11 (ITGA11), and the ITGA11 major ligand collagen type I α1 (COL1A1) among the 390 genes that were significantly enriched in NSCLC-associated CAFs. Increased ITGA11 expression in cancer stroma was correlated with a poor clinical outcome in patients with NSCLC. Increased expression of fibronectin and collagen type I induced ITGA11 expression in CAFs. The cellular migration of CAFs toward collagen type I and fibronectin was promoted via ERK1/2 signaling, independently of the fibronectin receptor integrin α5β1. Additionally, ERK1/2 signaling induced ITGA11 and COL11A1 expression in cancer stroma. We, therefore, propose that targeting ITGA11 and COL11A1 expressing CAFs to block cancer-stroma interactions may serve as a novel, promising anti-tumor strategy.

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Reactive Nitrogen Species Augment Fibroblast-Mediated Collagen Gel Contraction, Mediator Production, and Chemotaxis

Cited by 46 publications

References 34 publications

3-Nitrotyrosine inhibits fibroblast-mediated collagen gel contraction and chemotaxis

3-Nitrotyrosine inhibits fibroblast-mediated collagen gel contraction and chemotaxis

Recent developments in the role of reactive oxygen species in allergic asthma

Cancer‐associated fibroblast migration in non‐small cell lung cancers is modulated by increased integrin α11 expression

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