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Lung interstitial cells during alveolarization.

Choi CW - Korean J Pediatr (2010)

Bottom Line: To better understand this challenging complication, detailed alveolarization mechanisms should be delineated.Myofibroblasts are essential for secondary septation, a critical process of alveolarization, and localize to the front lines of alveologenesis.In this review, the role of lung interstitial cells during alveolarization and control mechanisms of their differentiation and migration will be discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.

ABSTRACT
Recent progress in neonatal medicine has enabled survival of many extremely low-birth-weight infants. Prenatal steroids, surfactants, and non-invasive ventilation have helped reduce the incidence of the classical form of bronchopulmonary dysplasia characterized by marked fibrosis and emphysema. However, a new form of bronchopulmonary dysplasia marked by arrest of alveolarization remains a complication in the postnatal course of extremely low-birth-weight infants. To better understand this challenging complication, detailed alveolarization mechanisms should be delineated. Proper alveolarization involves the temporal and spatial coordination of a number of cells, mediators, and genes. Cross-talk between the mesenchyme and the epithelium through soluble and diffusible factors are key processes of alveolarization. Lung interstitial cells derived from the mesenchyme play a crucial role in alveolarization. Peak alveolar formation coincides with intense lung interstitial cell proliferation. Myofibroblasts are essential for secondary septation, a critical process of alveolarization, and localize to the front lines of alveologenesis. The differentiation and migration of myofibroblasts are strictly controlled by various mediators and genes. Disruption of this finely controlled mechanism leads to abnormal alveolarization. Since arrest in alveolarization is a hallmark of a new form of bronchopulmonary dysplasia, knowledge regarding the role of lung interstitial cells during alveolarization and their control mechanism will enable us to find more specific therapeutic strategies for bronchopulmonary dysplasia. In this review, the role of lung interstitial cells during alveolarization and control mechanisms of their differentiation and migration will be discussed.

No MeSH data available.


Related in: MedlinePlus

Locations of myofibroblasts during lung development.
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Figure 1: Locations of myofibroblasts during lung development.

Mentions: Myofibroblasts lack lipid droplets and express smooth muscle actin. They are contractile cells and the source of septal elastin17). Myofibroblasts are located in developing secondary crests and at septal tips during the alveolar stage of lung development and are thus called alveolar myofibroblasts18). They are dual positive for elastin and smooth muscle actin in immunostaining assays, suggesting a role in elastin formation19). Alveolar myofibroblasts have morphologic and biochemical characteristics intermediate to fibroblasts and smooth muscle cells. During the pseudogladular stage of lung development, progenitors of alveolar myofibroblasts exist as a population of lung mesenchymal cells expressing platelet derived growth factor receptor (PDGFR)-α around the distal lung epithelial tubules and buds20). During the canalicular and saccular stages, these PDGFR-α-positive cells spread from their location around the distal epithelial buds to the walls of prospective terminal saccules to eventually become alveolar myofibroblasts (Fig. 1). Alveolar myofibroblasts are critical for secondary septa formation. Their absence is associated with a lack of secondary septation and the alveolarization failure21). Dysregulated myofibroblast development has been implicated in BPD22). Alveolar myofibroblasts are abundant during alveolarization, but are absent in adult lungs23). Because an excess of myofibroblasts is implicated in fibrotic diseases, alveolar myofibroblast disappearance following alveolarization completion may be critical. However, the regulatory mechanism of survival during alveolarization and subsequent disappearance of alveolar myofibroblasts is poorly understood.


Lung interstitial cells during alveolarization.

Choi CW - Korean J Pediatr (2010)

Locations of myofibroblasts during lung development.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3021730&req=5

Figure 1: Locations of myofibroblasts during lung development.
Mentions: Myofibroblasts lack lipid droplets and express smooth muscle actin. They are contractile cells and the source of septal elastin17). Myofibroblasts are located in developing secondary crests and at septal tips during the alveolar stage of lung development and are thus called alveolar myofibroblasts18). They are dual positive for elastin and smooth muscle actin in immunostaining assays, suggesting a role in elastin formation19). Alveolar myofibroblasts have morphologic and biochemical characteristics intermediate to fibroblasts and smooth muscle cells. During the pseudogladular stage of lung development, progenitors of alveolar myofibroblasts exist as a population of lung mesenchymal cells expressing platelet derived growth factor receptor (PDGFR)-α around the distal lung epithelial tubules and buds20). During the canalicular and saccular stages, these PDGFR-α-positive cells spread from their location around the distal epithelial buds to the walls of prospective terminal saccules to eventually become alveolar myofibroblasts (Fig. 1). Alveolar myofibroblasts are critical for secondary septa formation. Their absence is associated with a lack of secondary septation and the alveolarization failure21). Dysregulated myofibroblast development has been implicated in BPD22). Alveolar myofibroblasts are abundant during alveolarization, but are absent in adult lungs23). Because an excess of myofibroblasts is implicated in fibrotic diseases, alveolar myofibroblast disappearance following alveolarization completion may be critical. However, the regulatory mechanism of survival during alveolarization and subsequent disappearance of alveolar myofibroblasts is poorly understood.

Bottom Line: To better understand this challenging complication, detailed alveolarization mechanisms should be delineated.Myofibroblasts are essential for secondary septation, a critical process of alveolarization, and localize to the front lines of alveologenesis.In this review, the role of lung interstitial cells during alveolarization and control mechanisms of their differentiation and migration will be discussed.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea.

ABSTRACT
Recent progress in neonatal medicine has enabled survival of many extremely low-birth-weight infants. Prenatal steroids, surfactants, and non-invasive ventilation have helped reduce the incidence of the classical form of bronchopulmonary dysplasia characterized by marked fibrosis and emphysema. However, a new form of bronchopulmonary dysplasia marked by arrest of alveolarization remains a complication in the postnatal course of extremely low-birth-weight infants. To better understand this challenging complication, detailed alveolarization mechanisms should be delineated. Proper alveolarization involves the temporal and spatial coordination of a number of cells, mediators, and genes. Cross-talk between the mesenchyme and the epithelium through soluble and diffusible factors are key processes of alveolarization. Lung interstitial cells derived from the mesenchyme play a crucial role in alveolarization. Peak alveolar formation coincides with intense lung interstitial cell proliferation. Myofibroblasts are essential for secondary septation, a critical process of alveolarization, and localize to the front lines of alveologenesis. The differentiation and migration of myofibroblasts are strictly controlled by various mediators and genes. Disruption of this finely controlled mechanism leads to abnormal alveolarization. Since arrest in alveolarization is a hallmark of a new form of bronchopulmonary dysplasia, knowledge regarding the role of lung interstitial cells during alveolarization and their control mechanism will enable us to find more specific therapeutic strategies for bronchopulmonary dysplasia. In this review, the role of lung interstitial cells during alveolarization and control mechanisms of their differentiation and migration will be discussed.

No MeSH data available.


Related in: MedlinePlus