Lung Development and Adult Lung Diseases

CHEST Journal ◽  
2007 ◽  
Vol 132 (2) ◽  
pp. 651-656 ◽  
Author(s):  
Wei Shi ◽  
Saverio Bellusci ◽  
David Warburton
Keyword(s):  
Lung Development ◽  
Lung Diseases ◽  
Adult Lung

scholarly journals Unique Aspects of the Developing Lung Circulation: Structural Development and Regulation of Vasomotor Tone

2016 ◽  
Vol 6 (4) ◽  
pp. 407-425 ◽  
Author(s):  
Yuangsheng Gao ◽  
David N. Cornfield ◽  
Kurt R. Stenmark ◽  
Bernard Thébaud ◽  
Steven H. Abman ◽  
...  
Keyword(s):  
Lung Development ◽  
Lung Diseases ◽  
Vascular Tone ◽  
Current Knowledge ◽  
Normal Lung ◽  
Pulmonary Vasculature ◽  
Structural Development ◽  
Vasomotor Tone ◽  
Disease States ◽  
Vasculogenesis And Angiogenesis

This review summarizes our current knowledge on lung vasculogenesis and angiogenesis during normal lung development and the regulation of fetal and postnatal pulmonary vascular tone. In comparison to that of the adult, the pulmonary circulation of the fetus and newborn displays many unique characteristics. Moreover, altered development of pulmonary vasculature plays a more prominent role in compromised pulmonary vasoreactivity than in the adult. Clinically, a better understanding of the developmental changes in pulmonary vasculature and vasomotor tone and the mechanisms that are disrupted in disease states can lead to the development of new therapies for lung diseases characterized by impaired alveolar structure and pulmonary hypertension.

Neurotrophic factors and their receptors in lung development and implications in lung diseases

2021 ◽  
Author(s):  
Limor Rubin ◽  
Collin T. Stabler ◽  
Adi Schumacher-Klinger ◽  
Cezary Marcinkiewicz ◽  
Peter I. Lelkes ◽  
...  
Keyword(s):  
Neurotrophic Factors ◽  
Lung Development ◽  
Lung Diseases

scholarly journals In vitro models of fetal lung development to enhance research into congenital lung diseases

2021 ◽  
Author(s):  
Soichi Shibuya ◽  
Jessica Allen-Hyttinen ◽  
Paolo De Coppi ◽  
Federica Michielin
Keyword(s):  
Lung Development ◽  
Lung Diseases ◽  
Ex Vivo ◽  
Fetal Lung ◽  
Branching Morphogenesis ◽  
In Vitro Models ◽  
Normal Lung ◽  
Novel Therapeutic Strategies ◽  
Pseudoglandular Stage

Abstract Purpose This paper aims to build upon previous work to definitively establish in vitro models of murine pseudoglandular stage lung development. These can be easily translated to human fetal lung samples to allow the investigation of lung development in physiologic and pathologic conditions. Methods Lungs were harvested from mouse embryos at E12.5 and cultured in three different settings, i.e., whole lung culture, mesenchyme-free epithelium culture, and organoid culture. For the whole lung culture, extracted lungs were embedded in Matrigel and incubated on permeable filters. Separately, distal epithelial tips were isolated by firstly removing mesothelial and mesenchymal cells, and then severing the tips from the airway tubes. These were then cultured either in branch-promoting or self-renewing conditions. Results Cultured whole lungs underwent branching morphogenesis similarly to native lungs. Real-time qPCR analysis demonstrated expression of key genes essential for lung bud formation. The culture condition for epithelial tips was optimized by testing different concentrations of FGF10 and CHIR99021 and evaluating branching formation. The epithelial rudiments in self-renewing conditions formed spherical 3D structures with homogeneous Sox9 expression. Conclusion We report efficient protocols for ex vivo culture systems of pseudoglandular stage mouse embryonic lungs. These models can be applied to human samples and could be useful to paediatric surgeons to investigate normal lung development, understand the pathogenesis of congenital lung diseases, and explore novel therapeutic strategies.

scholarly journals Roles of Mesenchymal Cells in the Lung: From Lung Development to Chronic Obstructive Pulmonary Disease

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3467
Author(s):  
Amel Nasri ◽  
Florent Foisset ◽  
Engi Ahmed ◽  
Zakaria Lahmar ◽  
Isabelle Vachier ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Lung Development ◽  
Lung Diseases ◽  
Mesenchymal Cells ◽  
Chronic Obstructive ◽  
Multilineage Differentiation ◽  
Cell Type ◽  
Obstructive Pulmonary Disease ◽  
Lung Regeneration

Mesenchymal cells are an essential cell type because of their role in tissue support, their multilineage differentiation capacities and their potential clinical applications. They play a crucial role during lung development by interacting with airway epithelium, and also during lung regeneration and remodeling after injury. However, much less is known about their function in lung disease. In this review, we discuss the origins of mesenchymal cells during lung development, their crosstalk with the epithelium, and their role in lung diseases, particularly in chronic obstructive pulmonary disease.

Retinoid receptors in the developing human lung

2002 ◽  
Vol 103 (6) ◽  
pp. 613-621 ◽  
Author(s):  
Yuichiro KIMURA ◽  
Takashi SUZUKI ◽  
Chika KANEKO ◽  
Andrew D. DARNEL ◽  
Takuya MORIYA ◽  
...  
Keyword(s):  
Real Time ◽  
Quantitative Pcr ◽  
Lung Development ◽  
Thyroid Hormone Receptor ◽  
Fetal Lung ◽  
Mesenchymal Cells ◽  
Mrna Levels ◽  
Adult Lung ◽  
Real Time Quantitative Pcr ◽  
Retinoid Receptors

Nuclear receptors and their ligands are known to play very important roles in lung development. Among these receptors, retinoid receptors, members of the steroid/thyroid hormone receptor superfamily, are classified into retinoic acid receptor (RAR) isoforms α, β, and γ and retinoid X receptor (RXR) isoforms α, β, and γ. In addition, isoforms I and II of the orphan receptor chicken ovalbumin upstream promoter-transcription factor (COUP-TF) have been shown to negatively regulate the activation of retinoid receptors. Both of these receptors have been shown to regulate lung development in the mouse. In the present study we utilized immunohistochemistry and real-time quantitative PCR to examine the expression of RAR-α, -β and -γ, RXR-α, -β and -γ and COUP-TFII in the human fetal lung at 13–16 gestational weeks, a very critical stage of human pulmonary development, in order to study possible roles in pulmonary morphogenesis by comparing these findings with those of the adult lung. RXR-γ immunoreactivity was detected at both proximal (epithelia and mesenchyme of the trachea and bronchi associated with cartilage) and distal (epithelia and mesenchyme of smaller distal bronchi) sites in the fetal lung, but was markedly weaker in the adult lung. RAR-β immunoreactivity was detected in distal mesenchymal cells of the fetal lung, but was not discernible in distal mesenchymal cells in the adult lung (bronchioles, alveolar ducts and alveolus). Relatively intense RAR-γ immunoreactivity was detected in the chondrocytes of bronchial cells. COUP-TFII immunoreactivity was detected with a similar pattern to that of RAR-β. Real-time quantitative PCR analyses revealed that mRNA levels of RXR-γ at proximal and distal sites (ratio of fetal lung/adult lung: 3.4±0.05-fold and 3.1±0.03-fold respectively; P<0.01), RAR-β at distal sites (2.4±0.01-fold; P<0.05) and RAR-γ at proximal sites (2.2±0.11-fold; P<0.05) were significantly higher in the fetus than in the adult.

scholarly journals Arginine Therapy for Lung Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Jeremy A. Scott ◽  
Harm Maarsingh ◽  
Fernando Holguin ◽  
Hartmut Grasemann
Keyword(s):  
Nitric Oxide ◽  
Lung Development ◽  
Lung Diseases ◽  
Muscle Tone ◽  
Therapeutic Strategies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Nos Inhibitors ◽  
Inflammatory Processes ◽  
Vascular Smooth Muscle Tone

Nitric oxide (NO) is produced by a family of isoenzymes, nitric oxide synthases (NOSs), which all utilize L-arginine as substrate. The production of NO in the lung and airways can play a number of roles during lung development, regulates airway and vascular smooth muscle tone, and is involved in inflammatory processes and host defense. Altered L-arginine/NO homeostasis, due to the accumulation of endogenous NOS inhibitors and competition for substrate with the arginase enzymes, has been found to play a role in various conditions affecting the lung and in pulmonary diseases, such as asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), pulmonary hypertension, and bronchopulmonary dysplasia. Different therapeutic strategies to increase L-arginine levels or bioavailability are currently being explored in pre-clinical and clinical studies. These include supplementation of L-arginine or L-citrulline and inhibition of arginase.

scholarly journals Lung Development Genes and Adult Lung Function

2020 ◽  
Vol 202 (6) ◽  
pp. 853-865 ◽  
Author(s):  
Laura Portas ◽  
Miguel Pereira ◽  
Seif O. Shaheen ◽  
Annah B. Wyss ◽  
Stephanie J. London ◽  
...  
Keyword(s):  
Lung Function ◽  
Lung Development ◽  
Adult Lung

scholarly journals Insulin-Like Growth Factor-1 Signaling in Lung Development and Inflammatory Lung Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-27 ◽  
Author(s):  
Zheng Wang ◽  
Wenting Li ◽  
Qiongya Guo ◽  
Yuming Wang ◽  
Lijun Ma ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Development ◽  
Lung Diseases ◽  
Developmental Disorders ◽  
Biological Effects ◽  
Animal Experiments ◽  
Current Data ◽  
Alveolar Epithelial Cells ◽  
Insulin Like Growth Factor ◽  
Basal Cells

Insulin-like growth factor-1 (IGF-1) was firstly identified as a hormone that mediates the biological effects of growth hormone. Accumulating data have indicated the role of IGF-1 signaling pathway in lung development and diseases such as congenital disorders, cancers, inflammation, and fibrosis. IGF-1 signaling modulates the development and differentiation of many types of lung cells, including airway basal cells, club cells, alveolar epithelial cells, and fibroblasts. IGF-1 signaling deficiency results in alveolar hyperplasia in humans and disrupted lung architecture in animal models. The components of IGF-1 signaling pathways are potentiated as biomarkers as they are dysregulated locally or systemically in lung diseases, whereas data may be inconsistent or even paradoxical among different studies. The usage of IGF-1-based therapeutic agents urges for more researches in developmental disorders and inflammatory lung diseases, as the majority of current data are collected from limited number of animal experiments and are generally less exuberant than those in lung cancer. Elucidation of these questions by further bench-to-bedside researches may provide us with rational clinical diagnostic approaches and agents concerning IGF-1 signaling in lung diseases.

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