The pleural mesothelium in development and disease

Batra, Hitesh; Antony, Veena B.

doi:10.3389/fphys.2014.00284

Cited by 42 publications

(31 citation statements)

References 63 publications

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“…It has been proposed that postnatal PMCs contribute to the pathogenesis of pulmonary fibrosis by undergoing EMT to form fibroblasts or myofibroblasts (21). Evidence to support this hypothesis has come largely from analysis of cultured PMCs (13,22) and from analyses of marker gene expression in histological sections of human IPF samples and murine models (22).…”

Section: Discussionmentioning

confidence: 99%

Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis

Gise

Stevens

Honor

et al. 2016

Am J Respir Cell Mol Biol

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The lung is enveloped by a layer of specialized epithelium, the pulmonary mesothelium. In other organs, mesothelial cells undergo epithelialmesenchymal transition and contribute to organ stromal cells. The contribution of pulmonary mesothelial cells (PMCs) to the developing lung has been evaluated with differing conclusions. PMCs have also been indirectly implicated in lung fibrosis in the progressive, fatal lung disease idiopathic pulmonary fibrosis. We used fetal or postnatal genetic pulse labeling of PMCs to assess their fate in murine development, normal lung homeostasis, and models of pulmonary fibrosis. We found that most fetal PMC-derived mesenchymal cells (PMCDCs) expressed markers of pericytes and fibroblasts, only a small minority expressed smooth muscle markers, and none expressed endothelial cell markers. Postnatal PMCs did not contribute to lung mesenchyme during normal lung homeostasis or in models of lung fibrosis. However, fetal PMCDCs were abundant and actively proliferating within fibrotic regions in lung fibrosis models, suggesting that they actively participate in the fibrotic process. These data clarify the role of fetal and postnatal PMCDCs in lung development and disease.

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Section: Discussionmentioning

confidence: 99%

Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis

Gise

Stevens

Honor

et al. 2016

Am J Respir Cell Mol Biol

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“…Notably, cell fate mapping of WT1-expressing or lipophilic dye-labeled mesothelial cells show similar internal migration 26 and contribute to vascular smooth muscle and mesenchyme, including myofibroblasts, within lung and abdominal organs. 26,27 …”

Section: Discussionmentioning

confidence: 99%

Fetal Rat Gubernaculum Mesenchymal Cells Adopt Myogenic and Myofibroblast-Like Phenotypes

et al. 2016

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Purpose Gubernaculum-cremaster complex (GCC) development is hormonally-regulated and abnormal in a cryptorchid rat model. Using cell tracking techniques and imaging, we studied myogenic phenotypes and fates in the fetal rat GCC. Materials and methods E17 (embryonic day 17) GCCs were labeled with CellTracker™ or DNA synthesis marker 5-ethynyl-2′-deoxyuridine (EdU), or immobilized in Matrigel™ and grown in culture. E17-21 GCC sections and cells were imaged using widefield and deconvolution immunofluorescence microscopy and muscle- and/or myofibroblast-specific antibodies. Deconvolved image stacks were used to create a 3-dimensional (3D) model of E21 GCC muscle. Results Paired-box 7 (PAX7)+ and myogenin+ muscle precursors were visible in a desmin-rich “myogenic zone” between muscle layers that elongated and became thicker during development. GCC inner mesenchymal cells expressed desmin and alpha smooth muscle actin (αSMA) at lower levels than in the myogenic zone. After pulse-labeling with CellTracker™ or EdU, mesenchymal cells became incorporated into differentiated muscle. Conversely, mesenchymal cells migrated beyond Matrigel™-immobilized GCCs, expressed PAX7 and fused to form striated myotubes. Mesenchymal GCC cell lines proliferated >40 passages and exhibited contractile behavior, but did not form striated muscle. Our 3D GCC model showed 2 orthogonal ventral layers and an arcing inner layer of muscle. Conclusions Our data suggest that mesenchymal cells in the peripheral myogenic zone of the fetal GCC contribute to formation of a distinctively-patterned cremaster muscle. Non-myogenic, desmin- and αSMA-positive GCC mesenchymal cells proliferate and exhibit a myofibroblast-like phenotype in culture. Intrinsic mechanical properties of these divergent cell types may facilitate perinatal inversion of the GCC.

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“…Consequently, perturbation of barrier morphogenesis in childhood may have a lasting effect on adult epithelium via alteration of developmental programs and epigenetic reprogramming at developmental checkpoints 105–107 . Multiple lines of evidence now implicate active re-engagement of morphogenetic programs in adult disease, typically not seen in adult homeostatic tissue 108–110 . Alterations of the Wnt 66 , Hippo 111 , Notch/Jagged 112, 113 and Hedgehog 114 developmental pathways all exhibit strong association with epithelial remodeling and allergy.…”

Section: Mechanisms Of Barrier Defectsmentioning

confidence: 99%

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

Schleimer

Berdnikovs

2017

Journal of Allergy and Clinical Immunology

143

122

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Epithelial barriers of the skin, gastrointestinal tract and airway serve common critical functions such as maintaining a physical barrier against environmental insults and allergens, as well as providing a tissue interface balancing the communication between the internal and external environments. We now understand that in allergic disease, regardless of tissue location, the homeostatic balance of the epithelial barrier is skewed towards loss of differentiation, reduced junctional integrity and impaired innate defense. Importantly, epithelial dysfunction characterized by these traits appears to pre-date atopy and development of allergic disease. Despite our growing appreciation of the centrality of barrier dysfunction in the initiation of allergic disease, many important questions remain to be answered regarding the mechanisms disrupting the normal barrier function. Although our external environment (proteases, allergens, injury) is classically thought of as a principal contributor to barrier disruption associated with allergic sensitization, there is a need to better understand contributions of the internal environment (hormones, diet, circadian clock). Systemic drivers of disease, such as alterations of the endocrine system, metabolism and aberrant control of developmental signaling, are emerging as new players in driving epithelial dysfunction and allergic predisposition at various barrier sites. Identifying such central mediators of epithelial dysfunction, using both systems biology tools and causality-driven laboratory experimentation, will be essential in building new strategic interventions to prevent or reverse the process of barrier loss in allergy.

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The pleural mesothelium in development and disease

Cited by 42 publications

References 63 publications

Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis

Contribution of Fetal, but Not Adult, Pulmonary Mesothelium to Mesenchymal Lineages in Lung Homeostasis and Fibrosis

Fetal Rat Gubernaculum Mesenchymal Cells Adopt Myogenic and Myofibroblast-Like Phenotypes

Etiology of epithelial barrier dysfunction in patients with type 2 inflammatory diseases

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