Abstract
Mammalian lung development is a complex biological process, which is temporally and spatially regulated by growth factors, hormones, and extracellular matrix proteins. Abnormal changes of these molecules often lead to impaired lung development, and thus pulmonary diseases. Epithelial-mesenchymal interactions are crucial for fetal lung development. This paper reviews two interconnected pathways, pleiotrophin and Wnt/β-catenin, which are involved in fibroblast and epithelial cell communication during fetal lung development.
Highlights
Mammalian lung development is a complex biological process, which is temporally and spatially regulated by growth factors, hormones, and extracellular matrix proteins
1.2 Alveolar epithelial cell differentiation Alveolar epithelium is composed of two types of cells: alveolar epithelial type I cells (AEC I) and alveolar epithelial type II cells
PTN is a growth factor differentially expressed during fetal lung development
Summary
1.1 Stages of fetal lung development Fetal lung development is a complex biological process which involves temporal and spatial regulation of multiple factors such as growth factors, transcriptional factors, and extracellular matrix (ECM). The PTN receptor RPTPβ/ζ, is expressed in the airway epithelial cells at the late stages of fetal lung development. This suggests that PTN may mediate mesenchymal-epithelial interactions. Mouse double deficiency of Wnt and Wnt2b exhibits an underdeveloped lung which shows no trachea budding at E9.5, lacks the expression of TTF-1 (a transcription factor crucial for epithelial cell differentiation), and P63 (an esophagus epithelial marker) [98]. Apoptosis increases significantly in the vascular smooth muscle and epithelium following Wnt7b deprivation Another Wnt7b knockout mouse, Wnt7bD3, in which exon 3 is deleted, shows decreased proliferation of both epithelial and mesenchymal cells without perturbing cell differentiation and lung patterning [103].
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