Basement membrane and vascular remodelling in smokers and chronic obstructive pulmonary disease: a cross-sectional study

Soltani, Akbar; Reid, David W.; Sohal, Sukhwinder Singh; Wood‐Baker, Richard; Weston, S; Muller, H. Konrad; Walters, E. Haydn

doi:10.1186/1465-9921-11-105

Cited by 70 publications

(96 citation statements)

References 29 publications

(30 reference statements)

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“…In turn, activated endothelial cells upregulate expression of endothelial-cell-specific factors, including MMP14, that support growth of basal cells in the absence of exogenous growth factors. In vivo studies of smokingdependent airway remodeling demonstrate elevated expression of FGF2 in bronchial epithelial cells of patients with chronic obstructive pulmonary disease (COPD) (Kranenburg et al, 2005), enhanced expression of FGF and/or FGFR1 during vascular remodeling in COPD (Kranenburg et al, 2002), and altered distribution of vessels in the airway of smokers and smokers with COPD compared to healthy nonsmokers (Soltani et al, 2010). Therefore, crosstalk between basal cells and endothelial cells might play an important role in maintaining normal airway epithelial structure with alterations of this crosstalk contributing towards smoking-dependent airway remodeling.…”

Section: Resultsmentioning

confidence: 99%

Endothelial MMP14 is required for endothelial dependent growth support of human airway basal cells

Ding

Gomi

Rafii

et al. 2015

Journal of Cell Science

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Human airway basal cells are the stem (or progenitor) population of the airway epithelium, and play a central role in anchoring the epithelium to the basement membrane. The anatomic position of basal cells allows for potential paracrine signaling between them and the underlying nonepithelial stromal cells. In support of this, we have previously demonstrated that endothelial cells support growth of basal cells during co-culture through vascular endothelial growth factor A (VEGFA)-mediated signaling. Building on these findings, we found, by RNA sequencing analysis, that basal cells expressed multiple fibroblast growth factor (FGF) ligands (FGF2, FGF5, FGF11 and FGF13) and that only FGF2 and FGF5 were capable of functioning in a paracrine manner to activate classical FGF receptor (FGFR) signaling. Antibody-mediated blocking of FGFR1 during basal-cell-endothelialcell co-culture significantly reduced the endothelial-cell-dependent basal cell growth. Stimulation of endothelial cells with basal-cell-derived growth factors induced endothelial cell expression of matrix metallopeptidase 14 (MMP14), and short hairpin RNA (shRNA)-mediated knockdown of endothelial cell MMP14 significantly reduced the endothelial-cell-dependent growth of basal cells. Overall, these data characterize a new growth-factor-mediated reciprocal 'crosstalk' between human airway basal cells and endothelial cells that regulates proliferation of basal cells.

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Section: Resultsmentioning

confidence: 99%

Endothelial MMP14 is required for endothelial dependent growth support of human airway basal cells

Ding

Gomi

Rafii

et al. 2015

Journal of Cell Science

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“…Cells localised in the fragmentation area of the lamina reticularis poorly expressed cytokeratine, an epithelial marker, and S100A4 [141]. In addition, membrane fragmentation correlated with smoking history in COPD and stopping smoking could reduce the migratory capacity of fibroblastic cells [145]. These studies only used immunohistochemical staining from patient biopsies; therefore, the results do not show whether the cells identified as fibroblasts are from the migration of progenitor cells or from the ability of the epithelium to differentiate into fibroblast-like cells.…”

Section: Emt In Chronic Bronchial Diseases Emt and Allergic Asthmamentioning

confidence: 99%

Tissue remodelling in chronic bronchial diseases: from the epithelial to mesenchymal phenotype

Pain

Bermúdez

Lacoste

et al. 2014

European Respiratory Review

169

128

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Airway remodelling is a critical feature of chronic bronchial diseases, characterised by aberrant repair of the epithelium and accumulation of fibroblasts, which contribute to extracellular matrix (ECM) deposition resulting in fixed bronchial obstruction. Recently, epithelial-mesenchymal transition (EMT) has been identified as a new source of fibroblasts that could contribute to the remodelling of the airways. This phenomenon consists of the loss of the epithelial phenotype by bronchial epithelial cells and the acquisition of a mesenchymal phenotype. These cells are then able to migrate and secrete ECM molecules. Herein, we review the different types of EMT. We will then focus on the signalling pathways that are involved, such as transforming growth factor-b and Wnt, as well as the more recently described Sonic Hedgehog pathway. Finally, we will highlight the implication of EMT in airway remodelling in specific chronic bronchial pathologies, such as asthma, chronic obstructive pulmonary disease and bronchiolitis obliterans following lung transplantation. Despite the limitations of in vitro models, future studies of EMT in vivo are warranted to shed new light on the pathomechanisms of bronchial obstruction. @ERSpublications Epithelial-mesenchymal transition in chronic bronchial remodelling diseases

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“…Details of bronchoscopies and taking endobronchial biopsies have been described previously [16]. Eight biopsies from segmental bronchi in the right lower lobes were obtained from each individual.…”

Section: Methodsmentioning

confidence: 99%

“…We have previously reported hypervascularity in the reticular basement membrane (Rbm) and hypovascularity of the lamina propria (LP) in the airways of current smokers with COPD (S-COPD) and to some extent smokers with normal lung function (S-N) [16]. We questioned whether these vascular changes could be associated with alterations in the number of mast cells in these compartments, especially in close apposition to vessels.…”

mentioning

confidence: 96%

Mast cells in COPD airways: relationship to bronchodilator responsiveness and angiogenesis

Soltani

Ewe²,

Lim³

et al. 2011

Eur Respir J

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We have investigated whether mast cells are associated with bronchodilator responsiveness and airway vascular changes in chronic obstructive pulmonary disease (COPD) airways. We have previously shown that the reticular basement membrane is hypervascular and the lamina propria is hypovascular in COPD.Bronchial biopsies from 32 COPD subjects, 15 smokers with normal lung function and 17 controls, were immunostained for factor VIII, mast cell tryptase and chymase antibodies. Mast cells in the airway smooth muscle, the reticular basement membrane and the underlying lamina propria were quantitated.41% of COPD subjects had significant bronchodilator responsiveness, but this was not related to smooth muscle mast cell numbers. The reticular basement membrane had greater mast cell density in all groups compared with controls (p,0.01). In this compartment, perivascular mast cell density was related to hypervascularity. Lamina propria mast cell density was increased only in COPD (p,0.05). Perivascular mast cell density in the lamina propria was not related to its decreased vessel density.Bronchodilator responsiveness in COPD is not related to large airway smooth muscle mast cells of either type; both reticular basement membrane and lamina propria mast cells are increased in COPD patients, and perivascular mast cells may be involved in increased angiogenesis in the reticular basement membrane.

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Basement membrane and vascular remodelling in smokers and chronic obstructive pulmonary disease: a cross-sectional study

Cited by 70 publications

References 29 publications

Endothelial MMP14 is required for endothelial dependent growth support of human airway basal cells

Endothelial MMP14 is required for endothelial dependent growth support of human airway basal cells

Tissue remodelling in chronic bronchial diseases: from the epithelial to mesenchymal phenotype

Mast cells in COPD airways: relationship to bronchodilator responsiveness and angiogenesis

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