Mesenchymal-epithelial interactions in lung development and repair: are modeling and remodeling the same process?

DeMayo, Francesco J.; Minoo, Parviz; Plopper, Charles G.; Schuger, Lucia; Shannon, John M.; Torday, John S.

doi:10.1152/ajplung.00144.2002

Cited by 119 publications

(92 citation statements)

References 53 publications

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“…Many authors have thus conceptualized lung fi brosis as a form of aberrant repair. [9][10][11][12] In bleomycin-induced animal models, as well as in genetic models of surfactant disorders, apoptosis of the alveolar epithelium has been shown to be a critical early…”

Section: General Pathophysiology Of Ildmentioning

confidence: 99%

Pathogenesis of Interstitial Lung Disease in Children and Adults

Glasser¹,

Hardie²,

Hagood³

2010

Pediatric Allergy, Immunology, and Pulmonology

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Interstitial lung diseases (ILDs) occur across the lifespan, from birth to advanced age. However, the causes, clinical manifestations, histopathology, and management of ILD differ greatly among infants, older children, and adults. The historical approach of classifying childhood ILD (chILD) using adult classifi cation schemes may therefore have done more harm than good. Nevertheless, identifi cation of novel forms of chILD in the past decade, such as surfactant metabolism dysfunction disorders and neuroendocrine cell hyperplasia of infancy (NEHI), as well as genomic analysis of adult ILDs, has taught us that identical genotypes may result in distinct phenotypes at different ages and developmental stages, and that lung developmental pathways and cellular phenotypes are often recapitulated in adult ILDs. Thus comparison of the pathophysiology of ILD in children and adults in the context of lung development is useful in understanding the pathogenesis of these disorders, and may lead to novel therapeutic interventions for ILDs at all ages.

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Section: General Pathophysiology Of Ildmentioning

confidence: 99%

Pathogenesis of Interstitial Lung Disease in Children and Adults

Glasser¹,

Hardie²,

Hagood³

2010

Pediatric Allergy, Immunology, and Pulmonology

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show abstract

“…On the other hand, perturbations of NF-κB expression disrupt epithelial-mesenchymal interactions, resulting in abnormal lung morphogenesis. Thus NF-κB can modulate both inflammatory and morphological regulatory genes, establishing an operational and functional linkage between inflammation and development (60). Taken together, these data support a role for the reactivation of the epithelial-mesenchymal trophic unit as an important mechanism in chronic and severe asthma.…”

Section: Epithelial-mesenchymal Unitmentioning

confidence: 65%

Asthma: where is it going?

Faffe¹

2008

Braz J Med Biol Res

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Asthma is characterized by reversible airway obstruction, airway hyperresponsiveness, and airway inflammation. Although our understanding of its pathophysiological mechanisms continues to evolve, the relative contributions of airway hyperresponsiveness and inflammation are still debated. The first mechanism identified as important for asthma was bronchial hyperresponsiveness. In a second step, asthma was recognized also as an inflammatory disease, with chronic inflammation inducing structural changes or remodeling. However, persistence of airway dysfunction despite inflammatory control is observed in chronic severe asthma of both adults and children. More recently, a potential role for epithelial-mesenchymal communication or transition is emerging, with epithelial injury often resulting in a self-sustaining phenotype of wound repair modulation by activation/ reactivation of the epithelial-mesenchymal trophic unit, suggesting that chronic asthma can be more than an inflammatory disease. It is noteworthy that the gene-environmental interactions critical for the development of a full asthma phenotype involve processes similar to those occurring in branching morphogenesis. In addition, a central role for airway smooth muscle in the pathogenesis of the disease has been explored, highlighting its secretory function as well as different intrinsic properties compared to normal subjects. These new concepts can potentially shed light on the mechanisms underlying some asthma phenotypes and improve our understanding of the disease in terms of the therapeutic strategies to be applied. How we understand asthma and its mechanisms along time will be the focus of this overview.

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“…Lung development is controlled by two forces: intrinsic factors that include a host of regulatory molecules and extrinsic forces, and the main one being extracellular lung fluid (Demayo et al, 2002). The morphoregulatory molecules can be grouped into three classes: transcription factors (e.g., Nkx2.1 also known as thyroid transcription factor 1 (TTF-1), GATA, and HNF-3; signaling molecules, such as FGF, BMP-4, PDGF, Shh, and TGF-b; as well as extracellular matrix proteins and their receptors (Demayo et al, 2002;Shannon and Hyatt, 2004;Warburton et al, 2010;Maeda et al, 2007).…”

Section: Molecular Control Of Membrane-mediated Bgb Developmentmentioning

confidence: 99%

“…The morphoregulatory molecules can be grouped into three classes: transcription factors (e.g., Nkx2.1 also known as thyroid transcription factor 1 (TTF-1), GATA, and HNF-3; signaling molecules, such as FGF, BMP-4, PDGF, Shh, and TGF-b; as well as extracellular matrix proteins and their receptors (Demayo et al, 2002;Shannon and Hyatt, 2004;Warburton et al, 2010;Maeda et al, 2007). In mammals, extrinsic/mechanical forces have been shown to be important for fetal alveolar epithelial cell differentiation.…”

Section: Molecular Control Of Membrane-mediated Bgb Developmentmentioning

confidence: 99%

Membrane mediated development of the vertebrate blood‐gas‐barrier

Makanya

2016

Birth Defects Research Pt C

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During embryonic lung development, establishment of the gas‐exchanging units is guided by epithelial tubes lined by columnar cells. Ultimately, a thin blood‐gas barrier (BGB) is established and forms the interface for efficient gas exchange. This thin BGB is achieved through processes, which entail lowering of tight junctions, stretching, and thinning in mammals. In birds the processes are termed peremerecytosis, if they involve cell squeezing and constriction, or secarecytosis, if they entail cutting cells to size. In peremerecytosis, cells constrict at a point below the protruding apical part, resulting in fusion of the opposing membranes and discharge of the aposome, or the cell may be squeezed by the more endowed cognate neighbors. Secarecytosis may entail formation of double membranes below the aposome, subsequent unzipping and discharge of the aposome, or vesicles form below the aposome, fuse in a bilateral manner, and release the aposome. These processes occur within limited developmental windows, and are mediated through cell membranes that appear to be of intracellular in origin. In addition, basement membranes (BM) play pivotal roles in differentiation of the epithelial and endothelial layers of the BGB. Laminins found in the BM are particularly important in the signaling pathways that result in formation of squamous pneumocytes and pulmonary capillaries, the two major components of the BGB. Some information exists on the contribution by BM to BGB formation, but little is known regarding the molecules that drive peremerecytosis, or even the origins and composition of the double and vesicular membranes involved in secarecytosis. Birth Defects Research (Part C) 108:85–97, 2016. © 2016 Wiley Periodicals, Inc.

show abstract

Mesenchymal-epithelial interactions in lung development and repair: are modeling and remodeling the same process?

Cited by 119 publications

References 53 publications

Pathogenesis of Interstitial Lung Disease in Children and Adults

Pathogenesis of Interstitial Lung Disease in Children and Adults

Asthma: where is it going?

Membrane mediated development of the vertebrate blood‐gas‐barrier

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