Nerve growth factor induces type III collagen production in chronic allergic airway inflammation

Kılıç, Ayşe; Sonar, Sanchaita Sriwal; Yildirim, Ali Önder; Fehrenbach, Heinz; Nockher, Wolfgang Andreas; Renz, Harald

doi:10.1016/j.jaci.2011.06.017

Cited by 24 publications

(13 citation statements)

References 45 publications

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“…The involvement in wound repair may further suggest that this pathway is important in the regulation of airway remodelling in asthma. Indeed, in the study by Kilic et al [39] it was observed that blocking one of the neurotrophins, nerve growth factor (NGF), prevented subepithelial fibrosis in a mouse model of asthma and that NGF overexpression exerted a direct effect on collagen expression in murine lung fibroblasts. The involvement of neurotrophins in repair processes has been also confirmed recently by Palazzo et al [40] in wound healing in dermal fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

Altered microRNA expression profile during epithelial wound repair in bronchial epithelial cells

2013

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BackgroundAirway epithelial cells provide a protective barrier against environmental particles including potential pathogens. Epithelial repair in response to tissue damage is abnormal in asthmatic airway epithelium in comparison to the repair of normal epithelium after damage. The complex mechanisms coordinating the regulation of the processes involved in wound repair requires the phased expression of networks of genes. Small non-coding RNA molecules termed microRNAs (miRNAs) play a critical role in such coordinated regulation of gene expression. We aimed to establish if the phased expression of specific miRNAs is correlated with the repair of mechanically induced damage to the epithelium.MethodsTo investigate the possible involvement of miRNA in epithelial repair, we analyzed miRNA expression profiles during epithelial repair in a cell culture model using TaqMan-based quantitative real-time PCR in a TaqMan Low Density Array format. The expression of 754 miRNA genes at seven time points in a 48-hour period during the wound repair process was profiled using the bronchial epithelial cell line 16HBE14o- growing in monolayer.ResultsThe expression levels of numerous miRNAs were found to be altered during the wound repair process. These miRNA genes were clustered into 3 different patterns of expression that correlate with the further regulation of several biological pathways involved in wound repair. Moreover, it was observed that expression of some miRNA genes were significantly altered only at one time point, indicating their involvement in a specific stage of the epithelial wound repair.ConclusionsIn summary, miRNA expression is modulated during the normal repair processes in airway epithelium in vitro suggesting a potential role in regulation of wound repair.

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Section: Discussionmentioning

confidence: 99%

Altered microRNA expression profile during epithelial wound repair in bronchial epithelial cells

2013

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“…Primary lung fibroblasts were isolated from rodents following established protocols with minor modifications [60]. Briefly, lungs were perfused through the right ventricle of the heart with PBS and then excised and homogenized with GentleMACS (Miltenyi Biotec, Bergisch Gladbach, Germany), followed by collagenase D (2 mg ml −1 ; Roche, Indianapolis, IN, USA) treatment for 1 h at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

TAK1 inhibition attenuates both inflammation and fibrosis in experimental pneumoconiosis

Liang

Zhang

et al. 2017

Cell Discov

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Pneumoconiosis, caused by inhalation of mineral dusts, is a major occupational disease worldwide. Currently, there are no effective drugs owing to a lack of potential therapeutic targets during either the inflammation or fibrosis molecular events in pneumoconiosis. Here, we performed microarrays to identify aberrantly expressed genes in the above molecular events in vitro and found a hub gene transforming growth factor-β-activated kinase 1 (TAK1), which was highly expressed and activated in pneumoconiosis patients as well as silica-exposed rats with experimental pneumoconiosis. Genetic modulation of TAK1 by CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9, RNA interference and overexpression indicated the important role of TAK1 in both inflammation and fibrosis in experimental pneumoconiosis. To achieve pharmacological TAK1 inhibition, we virtually screened out a natural product resveratrol, which targeted TAK1 at both N161 and A107 residues, and significantly inhibited TAK1 activation to attenuate inflammation and fibrosis in vitro. Consistently, in vivo prevention and intervention studies showed that resveratrol could inhibit pulmonary inflammation and fibrosis in silica-exposed rats.

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“…When the visceral organs are inflamed or dysfunctional by diseases, NGF levels are often elevated in the viscera which then become a strong chemical cue acting on cells within the organ via a paracrine manner and/or act on the nerve terminals and sensitize the nervous system (Nazif et al, 2007; Yu et al, 2012; Qiao et al, 2013). In inflammatory states, NGF is a critical contributor in promoting excessive collagen production and deposition thereby resulting in poor compliance and stiffness of the organ (Chung et al, 2010; Kilic et al, 2011). In the urinary bladder with inflammation, endogenous NGF promotes type I collagen production through the MAPK and PI3K/Akt pathways (Chung et al, 2010).…”

Section: Neurotrophin Signaling In the Visceramentioning

confidence: 99%

“…In the urinary bladder with inflammation, endogenous NGF promotes type I collagen production through the MAPK and PI3K/Akt pathways (Chung et al, 2010). In chronic allergic airway inflammation, the increased NGF production contributes to type III collagen expression and deposition in the subepithelial compartment of the airways (Kilic et al, 2011). The novel role of NGF in regulating non-neuronal structure morphology is also suggested by transgenic overexpression of NGF in the organ which leads to excessive collagen deposition resulting in altered visceral physiology (Allen and Saban, 2010; Schnegelsberg et al, 2010; Kilic et al, 2011).…”

Section: Neurotrophin Signaling In the Visceramentioning

confidence: 99%

“…In chronic allergic airway inflammation, the increased NGF production contributes to type III collagen expression and deposition in the subepithelial compartment of the airways (Kilic et al, 2011). The novel role of NGF in regulating non-neuronal structure morphology is also suggested by transgenic overexpression of NGF in the organ which leads to excessive collagen deposition resulting in altered visceral physiology (Allen and Saban, 2010; Schnegelsberg et al, 2010; Kilic et al, 2011). NGF-regulated collagen production is mediated by the MAPK pathways involving the activation of ERK and p38, however, is independent of the traditional pathway involving the transforming growth factor beta (TGF-β)1/mothers against decapentaplegic homolog (SMAD) pathway (Kilic et al, 2011; Zhang and Qiao, 2012).…”

Section: Neurotrophin Signaling In the Visceramentioning

confidence: 99%

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Neurotrophin signaling and visceral hypersensitivity

Qiao

2014

Front. Biol.

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Neurotrophin family are traditionally recognized for their nerve growth promoting function and are recently identified as crucial factors in regulating neuronal activity in the central and peripheral nervous systems. The family members including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) are reported to have distinct roles in the development and maintenance of sensory phenotypes in normal states and in the modulation of sensory activity in disease. This paper highlights receptor tyrosine kinase (Trk) -mediated signal transduction by which neurotrophins regulate neuronal activity in the visceral sensory reflex pathways with emphasis on the distinct roles of NGF and BDNF signaling in physiologic and pathophysiological processes. Viscero-visceral cross-organ sensitization exists widely in human diseases. The role of neurotrophins in mediating neural cross talk and interaction in primary afferent neurons in the dorsal root ganglia (DRG) and neurotrophin signal transduction in the context of cross-organ sensitization are also discussed.

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Nerve growth factor induces type III collagen production in chronic allergic airway inflammation

Cited by 24 publications

References 45 publications

Altered microRNA expression profile during epithelial wound repair in bronchial epithelial cells

Altered microRNA expression profile during epithelial wound repair in bronchial epithelial cells

TAK1 inhibition attenuates both inflammation and fibrosis in experimental pneumoconiosis

Neurotrophin signaling and visceral hypersensitivity

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