Aberrant cell adhesion molecule expression in human bronchopulmonary sequestration and congenital cystic adenomatoid malformation

Volpe, MaryAnn V.; Chung, Eunice; Ulm, Jason P.; Gilchrist, Brian; Ralston, Steven J.; Wang, Karen T.; Nielsen, Heber C.

doi:10.1152/ajplung.90618.2008

Cited by 28 publications

(20 citation statements)

References 72 publications

(97 reference statements)

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“…These data suggest that one role for β1 integrin-mediated cell-matrix interactions in the lung is to restrict epithelial cell multilayering and promote proper apical-basal epithelial polarity. Interestingly, β1 integrins and other cell adhesion molecules, including E-cadherin (cadherin 1), are aberrantly expressed in certain congenital lung abnormalities, such as bronchopulmonary sequestration and congenital cystic adenomatoid malformations (Volpe et al, 2009). Further exploration of cell-matrix interactions during the development of the airways will probably uncover additional insights into how lung epithelial cells are organized to give rise to the appropriate architecture of the branched airway network.…”

Section: Branching Morphogenesis and Epithelial Organization Of The Lungmentioning

confidence: 99%

Lung development: orchestrating the generation and regeneration of a complex organ

2014

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The respiratory system, which consists of the lungs, trachea and associated vasculature, is essential for terrestrial life. In recent years, extensive progress has been made in defining the temporal progression of lung development, and this has led to exciting discoveries, including the derivation of lung epithelium from pluripotent stem cells and the discovery of developmental pathways that are targets for new therapeutics. These discoveries have also provided new insights into the regenerative capacity of the respiratory system. This Review highlights recent advances in our understanding of lung development and regeneration, which will hopefully lead to better insights into both congenital and acquired lung diseases. KEY WORDS: Branching morphogenesis, Epigenetics, Lung, Regeneration IntroductionThe primary function of the lungs is to exchange oxygen in the external environment with carbon dioxide in the cardiovascular system. Although this process sounds straightforward, it is fraught with multiple barriers to its success. The entire airway, like the skin, is constantly exposed to the external environment and must cope with challenges including temperature, particulate matter and allergens. Terrestrial life has adapted to these and other challenges through the evolution of a complex respiratory system consisting of a multitude of cell lineages. These cellular components are constantly communicating with each other to exchange gas efficiently while preventing blood and fluid loss and dangerous infection from pathogens.Lung development has been studied extensively in recent years, generating new insights into the origins of the different cell lineages that exist in the lung as well as the molecular pathways that regulate these lineages. This has led to novel insights into congenital lung diseases, lung abnormalities and acquired lung diseases (Box 1), including asthma and chronic obstructive pulmonary disease (COPD), and the lung's response to acute injury. In addition, these studies have revealed that some cell lineages within the mammalian respiratory system can regenerate after injury through the activation of stem/progenitor populations or through proliferation-induced cellular expansion. The molecular pathways that regulate these regenerative processes have been identified, raising the hope that these can be harnessed to promote lung regeneration in humans. Moreover, using the robust knowledge of pathways that regulate early lung development, lung epithelial cells can now be generated from embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), providing an additional source of cells for disease modeling and potential cell-based therapies (Longmire et al., 2012;Mou et al., 2012). In this Review, we highlight recent advances in the basic understanding of lung development and regeneration with a focus on the cell biology of the developing lung epithelium, the role of endoderm progenitors, and the epigenetic regulation of lung development and regeneration. We also discuss how these adv...

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Section: Branching Morphogenesis and Epithelial Organization Of The Lungmentioning

confidence: 99%

Lung development: orchestrating the generation and regeneration of a complex organ

2014

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“…An overexpression of Clara cell marker 10 was also identified [13]. Altered integrin cytoplasmic signalling was also proposed, since integrin and E-cadherin expression patterns were altered in CPAM tissue [35]. …”

Section: Histopathology and Geneticsmentioning

confidence: 99%

“…2 Genes implicated in CPAM, PPB and BAC [14,30,31,32,33,34,35,127,137,138,139,140,141,142,143]. TTF1 = Thyroid transcription factor 1; PDGF-B = platelet-derived growth factor B; FABP-7 = fatty acid-binding protein 7; GDNF = glial cell-derived neurotrophic factor; Shh = sonic hedgehog; FGFR2b = FGF receptor-2b; FHIT = fragile histidine triad; Rb = retinoblastoma protein; EGFR = epidermal growth factor receptor. …”

Section: Managementmentioning

confidence: 99%

Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation

2016

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Congenital pulmonary airway malformation (CPAM) is one of the most common lung lesions detected prenatally. Despite the research efforts made in the past few years, controversy and lack of clarity in the literature still exist regarding nomenclature, classification, pathogenesis and the management of CPAM. Therefore, it is of greatest importance to delineate the natural history of CPAMs and to create a consensus to guide the management and follow-up of these lesions. This review will focus on classification systems, highlighting the most recent advancements in pathogenesis, and current practice in the prenatal diagnosis of CPAM. Strategies of prenatal management and postnatal management will be reviewed. Long-term follow-up, including lung cancer risk, is discussed and an outcome perspective is presented.

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“…Specific cell adhesion molecules are important to lung development and airway morphogenesis. E-cadherin protein level was significantly upregulated in congenital lung lesions with abnormal airway branching [11]. Whereas, reduced production of the vasodilator nitric oxide (NO) in fetal vessels in pregnant smokers may lower the blood flow to the fetus and result in lower birth weight, length, and head circumference [12].…”

Section: Introductionmentioning

confidence: 99%

Clinical and Biochemical Effects of Environmental Tobacco Smoking On Pregnancy Outcome

et al. 2012

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The effects of environmental tobacco smoke (ETS) are less studied especially on neonates. This study evaluates the clinical and biochemical effects in neonates exposed to ETS during pregnancy. Two hundred pregnant women asked to complete the questioners about their ETS. Ninety from them were enrolled in biochemical assays as two groups according to ETS. The cotinine level determined in saliva and serum of mothers to confirm their tobacco exposure. The routine tracheal suction from the fetus was used to determine the level of neuron specific enolase (NSE), soluble E-cadherin, sApo-1/Fas, nitric oxide (NO) and cotinine. In clinical assessment, the percent of full term babies in nonexposed group (72 %) are higher compared to exposed group (67 %). Apgar score at the first min, admission to intensive care unit (ICU) and morbidity during the first month shows statistical significance increase in exposed compared to non-exposed group (p = 0.03, 0.05, 0.01, respectively). The new born weight in exposed group significantly decreased compared to non-exposed group (2,850 g ± 3.74 vs 2,967.67 g ± 3.34; p = 0.02). In biochemical assessment, NSE and sE-cadherin significantly increased, while NO significantly decreased (p = 0.000) in exposed compared to non-exposed group. There is a positive correlation between level of cotinine and both NSE, sE-cadherin (r = 0.7, 0.9; p = 0.000, 0.006, respectively). To our knowledge, this is the first study link between prenatal tobacco exposure (PTE) and biochemical parameters measured in tracheal suction. PTE will lead to decrease in birth weight most probably by decreasing NO, sFas, and increasing sE-cadherin. While, increased morbidity of neonates in the exposed group could be attributed to cessation of breast feeding and its complication and increased NSE in the studied markers.

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Aberrant cell adhesion molecule expression in human bronchopulmonary sequestration and congenital cystic adenomatoid malformation

Cited by 28 publications

References 72 publications

Lung development: orchestrating the generation and regeneration of a complex organ

Lung development: orchestrating the generation and regeneration of a complex organ

Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation

Clinical and Biochemical Effects of Environmental Tobacco Smoking On Pregnancy Outcome

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