Release of biologically active TGF-β from airway smooth muscle cells induces autocrine synthesis of collagen

Coutts, Amanda S.; Chen, Gang; Stephens, N. L.; Hirst, Stuart J John; Douglas, Deborah; Eichholtz, Thomas; Khalil, Nasreen

doi:10.1152/ajplung.2001.280.5.l999

Cited by 105 publications

(94 citation statements)

References 35 publications

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“…It is possible that DC express insufficient MIF and, therefore, the MIF-related effects are not strongly mediated by these cells. Moreover, it is known that other cells such as eosinophils and airway epithelial and SMC also produce MIF (18,19) (Fig. 1B) and, therefore, the role of BMMC-or Mderived MIF in T cell activation/proliferation observed from our in vitro pure cell population assay (Fig.…”

Section: Mast Cell-derived Mif Is Required For Airway Inflammationmentioning

confidence: 77%

“…1E). Another hallmark of airway inflammation is increased cell proliferation mediated by TGF-␤ from eosinophils (18) or airway SMC (19). In vitro experiments demonstrated that TGF-␤ induces MIF expression in murine colon carcinoma cells (20) and, in turn, MIF regulates TGF-␤ expression in mesangial cells (21).…”

Section: Mif-deficient Balf or Serum Contains Reduced Levels Of Chemomentioning

confidence: 99%

See 1 more Smart Citation

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

Wang

Huang

Wolters

et al. 2006

The Journal of Immunology

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Increased levels of macrophage migration inhibitory factor (MIF) in serum, sputum, and bronchioalveolar lavage fluid (BALF) from asthmatic patients and time/dose-dependent expression of MIF in eosinophils in response to phorbol myristate acetate suggest the participation of MIF in airway inflammation. In this study, we examined inflammation in OVA-sensitized mouse lungs in wild-type and MIF-deficient mice (MIF−/−). We report increased MIF in the lung and BALF of sensitized wild-type mice. MIF−/− mice demonstrated significant reductions in serum IgE and alveolar inflammatory cell recruitment. Reduced Th1/Th2 cytokines and chemokines also were detected in serum or BALF from MIF−/− mice. Importantly, alveolar macrophages and mast cells, but not dendritic cells or splenocytes, from MIF−/− mice demonstrated impaired CD4+ T cell activation, and the reconstitution of wild-type mast cells in MIF−/− mice restored the phenotype of OVA-induced airway inflammation, revealing a novel and essential role of mast cell-derived MIF in experimentally induced airway allergic diseases.

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Section: Mast Cell-derived Mif Is Required For Airway Inflammationmentioning

confidence: 77%

Section: Mif-deficient Balf or Serum Contains Reduced Levels Of Chemomentioning

confidence: 99%

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

Wang

Huang

Wolters

et al. 2006

The Journal of Immunology

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“…For example, increased TGF-b1 levels are associated with increased airway remodeling but decreased airways responsiveness in transgenic mice over-expressing TGFB1 in the lungs (42). In humans, TGF-b1 has been shown to stimulate increased synthesis of fibronectin/collagen (26,27), stimulate smooth muscle proliferation in the airways of people with asthma (by increasing both smooth muscle cell size and number) (43), and enhance immune responses against viral illnesses (44). Thus, genetic variants that lead to reduced levels of TGF-b1 could theoretically have paradoxical effects on airway remodeling and airway responsiveness in subjects with asthma.…”

Section: Discussionmentioning

confidence: 99%

Variants in TGFB1, Dust Mite Exposure, and Disease Severity in Children with Asthma

Sharma¹,

Raby²,

Hunninghake³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Polymorphisms in the gene for transforming growth factor-b1 (TGFB1) have been associated with asthma, but not with airway responsiveness or disease exacerbations in subjects with asthma. Objectives: To test for association between single nucleotide polymorphisms (SNPs) in TGFB1 and markers of asthma severity in childhood. Methods: We tested for the association between nine SNPs in TGFB1 and indicators of asthma severity (lung function, airway responsiveness, and disease exacerbations) in two cohorts: 416 Costa Rican parent-child trios and 465 families of non-Hispanic white children in the Childhood Asthma Management Program (CAMP). We also tested for the interaction between these polymorphisms and exposure to dust mite allergen on asthma severity. Measurements and Main Results: The A allele of promoter SNP rs2241712 was associated with increased airway responsiveness in Costa Rica (P 5 0.0006) and CAMP (P 5 0.005), and the C allele of an SNP in the promoter region (rs1800469) was associated with increased airway responsiveness in both cohorts (P < 0.01). Dust mite exposure modified the effect of the C allele of exonic SNP rs1800471 on airway responsiveness (P 5 0.03 for interactions in both cohorts). The T allele of a coding SNP (rs1982073) was associated with a reduced risk of asthma exacerbations in Costa Rica (P 5 0.009) and CAMP (P 5 0.005). Dust mite exposure also significantly modified the effect of the A allele of the promoter SNP rs2241712 on asthma exacerbations in both cohorts. Conclusions: SNPs in TGFB1 are associated with airway responsiveness and disease exacerbations in children with asthma. Moreover, dust mite exposure may modify the effect of TGFB1 SNPs on airway responsiveness and asthma exacerbations.

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“…Furthermore, activation of avß6 may modulate AHR by altering the expression of mast-cell proteases that can contribute to or inhibit airway narrowing (63). In addition, proteases can cleave latent TGF-b1 into its active form, inducing the synthesis of collagen in an autocrine fashion (64). Other mechanisms of TGF-b1 activation, such as ROS, mechanical stretch, contraction, and even extreme temperature changes, may also be pivotal to contributing to TGF-b1-induced fibrotic responses in asthma (Table 1).…”

Section: Airway Remodeling and Proliferationmentioning

confidence: 99%

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

Ojiaku

Yoo

Panettieri

2017

Am J Respir Cell Mol Biol

106

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The pathogenesis of asthma includes a complex interplay among airway inflammation, hyperresponsiveness, and remodeling. Current evidence suggests that airway structural cells, including bronchial smooth muscle cells, myofibroblasts, fibroblasts, and epithelial cells, mediate all three aspects of asthma pathogenesis. Although studies show a connection between airway remodeling and changes in bronchomotor tone, the relationship between the two remains unclear. Transforming growth factor b1 (TGF-b1), a growth factor elevated in the airway of patients with asthma, plays a role in airway remodeling and in the shortening of various airway structural cells. However, the role of TGF-b1 in mediating airway hyperresponsiveness remains unclear. In this review, we summarize the literature addressing the role of TGF-b1 in airway remodeling and shortening. Through our review, we aim to further elucidate the role of TGF-b1 in asthma pathogenesis and the link between airway remodeling and airway hyperresponsiveness in asthma and to define TGF-b1 as a potential therapeutic target for reducing asthma morbidity and mortality.

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Release of biologically active TGF-β from airway smooth muscle cells induces autocrine synthesis of collagen

Cited by 105 publications

References 35 publications

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

Cutting Edge: Deficiency of Macrophage Migration Inhibitory Factor Impairs Murine Airway Allergic Responses

Variants in TGFB1, Dust Mite Exposure, and Disease Severity in Children with Asthma

Transforming Growth Factor β1 Function in Airway Remodeling and Hyperresponsiveness. The Missing Link?

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