Fibronectin and Hyaluronan in Bronchoalveolar Lavage Fluid from Young Patients with Chronic Obstructive Pulmonary Diseases

Song, Wei; Zhang, An Cheng; Pang, Yu Ying; Liu, Li Hua; Zhao, Jiyun; Deng, Shu Hua; Zhang, Shi Yuan

doi:10.1159/000196406

Cited by 24 publications

(18 citation statements)

References 20 publications

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“…Fibronectin is found elevated and has been implicated in the pathogenesis of obstructive lung diseases like asthma (9,43,47). Its expression in lung is stimulated by transforming growth factor-␤1 and other growth factors present in serum (27,36).…”

Section: Adenosine Stimulates the Expression Of Fibronectin In A549 Cmentioning

confidence: 99%

“…This work focuses on fibronectin, a matrix glycoprotein highly expressed in injured tissues that has been implicated in wound healing and repair (24,39). Fibronectin is increased in the alveolar lining fluid of smokers and subjects with chronic obstructive lung disease (43,47). In the asthmatic airway, fibronectin deposition is increased in the subepithelial layer (37).…”

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confidence: 99%

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Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling

Roman

Rivera²,

Roser‐Page³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Adenosine is an extracellular nucleoside that is elevated in tissues during hypoxia and ischemia reperfusion and has been implicated in asthma and other lung disorders. There, adenosine is considered an important modulator of physiological functions and inflammation, but its effects on matrix expression and turnover during tissue remodeling are unknown. We examined the effects of adenosine on lung epithelial cells with particular attention to the expression of fibronectin, a matrix glycoprotein highly expressed in injured tissues that has been implicated in wound healing. In A549 lung epithelial cells, we found that adenosine induced expression of fibronectin mRNA and protein in a dose- and time-dependent manner and found that the stimulatory effect of adenosine was inhibited by specific adenosine receptor antagonists. Adenosine stimulation was associated with increased levels of intracellular cAMP and with phosphorylation and DNA binding of the cAMP response element binding protein (CREB), known for its ability to stimulate fibronectin gene transcription. To confirm the latter, A549 cells were transfected with a DNA construct containing the human fibronectin promoter connected to a luciferase reporter gene. Adenosine stimulated transcription of the gene, and this effect was blocked by inhibitors of protein kinase activation. Finally, we tested primary lung fibroblasts and primary alveolar epithelial type II cells and found increased fibronectin expression in response to adenosine. Overall, our observations suggest that adenosine might modulate tissue remodeling by stimulating fibronectin expression in lung epithelial cells through induction of purinergic receptor-mediated signals that target CREB phosphorylation and stimulate fibronectin gene transcription.

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Section: Adenosine Stimulates the Expression Of Fibronectin In A549 Cmentioning

confidence: 99%

mentioning

confidence: 99%

Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling

Roman

Rivera²,

Roser‐Page³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Although it differs chemically from fibronectin, vitronectin has very similar functions in that both proteins interact with macromolecules, including fibrin, collagen, proteoglycans, and promote cell proliferation, cytodifferentiation and migration [5, 6]. Vitronectin is a useful marker of profibrotic activity [7].…”

Section: Introductionmentioning

confidence: 99%

Increased Vitronectin and Endothelin-1 in the Breath Condensate of Patients with Fibrosing Lung Disease

Carpagnano

Kharitonov²,

Wells³

et al. 2003

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Background: Non-specific interstitial pneumonia (NSIP) and fibrosing alveolitis associated with systemic sclerosis (FASSc) are diseases of unknown aetiology that are characterised by the accumulation of mononuclear cells, followed by the progressive deposition of collagen within the interstitium and subsequent destruction of lung airspace. Better understanding of mediators involved in fibrosis may be useful for early diagnosis and in clinical monitoring of disease progression. Objective: The aim of this study was to investigate the presence of two profibrotic markers, the vitronectin and the endothelin-1 (ET-1) in the airways of NSIP and FASSc patients. Methods: Ten NSIP (6 males, age 57 ± 2 years) and 15 FASSc (8 males, age 55 ± 4 years) patients were recruited along with 10 normal subjects (4 male, age 52 ± 2 years). Vitronectin and ET-1 concentrations were measured in their breath condensate, using a specific enzyme immunoassay. Results: Higher levels of vitronectin and ET-1 were observed in NSIP and FASSc patients [median 92.8 (91.7–93.9) µg/ml; median 8.3 (7.9–9.3) pg/ml] than in control subjects [median 80.3 (89.3–91.4) µg/ml; p < 0.01; median 5.3 (4.9–5.9) pg/ml, p < 0.0001]. We also found increased concentrations of vitronectin in patients with clinical deterioration compared to those remaining stable and in ex-smokers compared to non-smokers and, increased vitronectin and ET-1 in patients treated with steroids compared to untreated patients. Conclusion: These findings justify further studies of vitronectin and ET-1 levels in exhaled breath condensate, as a means of monitoring activity and predicting progression of pulmonary fibrosis.

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“…In fact, various extracellular matrix components, such as hyaluronan (HA), are found in increased concentrations in bronchoalveolar fluid from patients with chronic airway inflammation and are used as a marker of inflammation (35,42). HA, a negatively charged high-molecular-weight glycosaminoglycan made up of repeating disaccharide units, is ubiquitously distributed in the extracellular matrix (24,25).…”

mentioning

confidence: 99%

Differential regulation of hyaluronan-induced IL-8 and IP-10 in airway epithelial cells

Boodoo

Spannhake

Powell

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Airway epithelium is emerging as a regulator of local inflammation and immune responses. However, the cellular and molecular mechanisms responsible for the immune modulation by these cells have yet to be fully elucidated. At the cellular level, the hallmarks of airway inflammation are mucus gland hypertrophy with excess mucus production, accumulation of inflammatory mediators, inflammation in the airway walls and lumen, and breakdown and turnover of the extracellular matrix. We demonstrate that fragments of the extracellular matrix component hyaluronan induce inflammatory chemokine production in primary airway epithelial cells grown at an air-liquid interface. Furthermore, hyaluronan fragments use two distinct molecular pathways to induce IL-8 and IFN-γ-inducible protein 10 (IP-10) chemokine expression in airway epithelial cells. Hyaluronan-induced IL-8 requires the MAP kinase pathway, whereas hyaluronan-induced IP-10 utilizes the NF-κB pathway. The induction is specific to low-molecular-weight hyaluronan fragments as other glycosaminoglycans do not induce IL-8 and IP-10 in airway epithelial cells. We hypothesize that not only is the extracellular matrix a target of destruction in airway inflammation but it plays a critical role in perpetuating inflammation through the induction of cytokines, chemokines, and modulatory enzymes in epithelial cells. Furthermore, hyaluronan, by inducing IL-8 and IP-10 by distinct pathways, provides a unique target for differential regulation of key inflammatory chemokines.

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Fibronectin and Hyaluronan in Bronchoalveolar Lavage Fluid from Young Patients with Chronic Obstructive Pulmonary Diseases

Cited by 24 publications

References 20 publications

Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling

Adenosine induces fibronectin expression in lung epithelial cells: implications for airway remodeling

Increased Vitronectin and Endothelin-1 in the Breath Condensate of Patients with Fibrosing Lung Disease

Differential regulation of hyaluronan-induced IL-8 and IP-10 in airway epithelial cells

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