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

Gao, Yuangsheng; Cornfield, David N.; Stenmark, Kurt R.; Thébaud, Bernard; Raj, J. Usha

doi:10.1086/688890

Cited by 42 publications

(29 citation statements)

References 243 publications

(548 reference statements)

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“…During normal lung development angiogenesis is coordinated precisely, leading to a balance in factors that promote expansion with those that promote stability of the endothelial barrier [30,31]. Normal alveolar development has been shown to be dependent on angiogenesis [4,32,33] and dysregulated vascular growth is a well-established feature of the BPD phenotype [1,4].…”

Section: Discussionmentioning

confidence: 99%

“…Regulation of the balance of vascular growth factors in the developing lung is known to be critical in the creation of the extensive network of blood vessels necessary to support alveolarization [30,31]. The Ang-Tie2 axis has been shown to play an essential role in maintaining both vascular homeostasis and expansion during lung development [31,40].…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

et al. 2020

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Background: Macrophage migration inhibitory factor (MIF) has been implicated as a protective factor in the development of bronchopulmonary dysplasia (BPD) and is known to be regulated by . The aim of this study was to evaluate the role of miR-451 and the MIF signaling pathway in in vitro and in vivo models of BPD. Methods: Studies were conducted in mouse lung endothelial cells (MLECs) exposed to hyperoxia and in a newborn mouse model of hyperoxia-induced BPD. Lung and cardiac morphometry as well as vascular markers were evaluated. Results: Increased expression of miR-451 was noted in MLECs exposed to hyperoxia and in lungs of BPD mice. Administration of a miR-451 inhibitor to MLECs exposed to hyperoxia was associated with increased expression of MIF and decreased expression of angiopoietin (Ang) 2. Treatment with the miR-451 inhibitor was associated with improved lung morphometry indices, significant reduction in right ventricular hypertrophy, decreased mean arterial wall thickness and improvement in vascular density in BPD mice. Western blot analysis demonstrated preservation of MIF expression in BPD animals treated with a miR-451 inhibitor and increased expression of vascular endothelial growth factor-A (VEGF-A), Ang1, Ang2 and the Ang receptor, Tie2. Conclusion: We demonstrated that inhibition of miR-451 is associated with mitigation of the cardio-pulmonary phenotype, preservation of MIF expression and increased expression of several vascular growth factors.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

et al. 2020

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“…Angiogenesis follows, and is responsible for the remodelling and expansion of the pulmonary vascular network through both endothelial sprouting and intussusceptive growth (Peng & Morrisey, ; Gao et al . ). During the canalicular stage of lung development (human gestation weeks 16–26), there is a dramatic rise in the number of lung capillaries to form the first air–blood interface, which continue to mature during the saccular stage (weeks 24–38).…”

Section: Normal Vascular Developmentmentioning

confidence: 97%

“…Left‐to‐right shunts, as seen in septal defects or patent ductus arteriosus, may accentuate pulmonary vascular sheer stress and promote vascular remodelling (Gao et al . ).…”

Section: Impaired Pulmonary Vascularizationmentioning

confidence: 97%

Long‐term pulmonary vascular consequences of perinatal insults

Goss

2018

The Journal of Physiology

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Development of the pulmonary circulation is a critical component of fetal lung development, and continues throughout infancy and childhood, marking an extended window of susceptibility to vascular maldevelopment and maladaptation. Perinatal vascular insults may result in abnormal vascular structure or function, including decreased angiogenic signaling and vascular endowment, impaired vasoreactivity through increased pulmonary artery endothelial dysfunction and remodeling, or enhanced genetic susceptibility to pulmonary vascular disease through epigenetic modifications or germline mutations. Although some infants develop early onset pulmonary hypertension, due to the unique adaptive capabilities of the immature host many do not have clinically evident early pulmonary vascular dysfunction. These individuals remain at increased risk for development of late-onset pulmonary hypertension, and may be particularly susceptible to secondary insults. This review will address the role of perinatal vascular insults in the development of late pulmonary vascular dysfunction with an effort to highlight areas of critical research need.

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“…; Gao et al . ). After a primary vascular plexus is formed, angiogenesis takes over as new capillaries sprout from the primary vascular structures constructed by differentiated endothelial cells.…”

Section: Introductionmentioning

confidence: 97%

Angiogenesis in the lung

Eldridge

Wagner

2018

The Journal of Physiology

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Both systemic (tracheal and bronchial) and pulmonary circulations perfuse the lung. However, documentation of angiogenesis of either is complicated by the presence of the other. Well-documented angiogenesis of the systemic circulations have been identified in asthma, cystic fibrosis, chronic thromboembolism and primary carcinomas. Angiogenesis of the vasa vasorum, which are branches of bronchial arteries, is seen in the walls of large pulmonary vessels after a period of chronic hypoxia. Documentation of increased pulmonary capillaries has been shown in models of chronic hypoxia, after pneumonectomy and in some carcinomas. Although endothelial cell proliferation may occur as part of the repair process in several pulmonary diseases, it is separate from the unique establishment of new functional perfusing networks defined as angiogenesis. Identification of the mechanisms driving the expansion of new vascular beds in the adult needs further investigation. Yet the growth factors and molecular mechanisms of lung angiogenesis remain difficult to separate from underlying disease sequelae.

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

Cited by 42 publications

References 243 publications

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

Inhibition of microRNA-451 is associated with increased expression of Macrophage Migration Inhibitory Factor and mitigation of the cardio-pulmonary phenotype in a murine model of Bronchopulmonary Dysplasia

Long‐term pulmonary vascular consequences of perinatal insults

Angiogenesis in the lung

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