Vascular Niche in Lung Alveolar Development, Homeostasis, and Regeneration

Mammoto, Akiko; Mammoto, Tadanori

doi:10.3389/fbioe.2019.00318

Cited by 56 publications

(44 citation statements)

References 186 publications

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“…We used Tie2-specific Twist1 knockout mice in this study and found that Twist1 knockdown in Tie2-expressing cells restores regenerative lung growth in the aged mouse lungs. Since Tie2 is expressed in other cell types such as fibroblasts and immune cells, which also contribute to vascular and alveolar epithelial morphogenesis [ 69 ], Twist1 expression in these other cells may contribute to post-PNX lung growth in the aged lung. Twist1 knockdown in ECs in other organs may also indirectly affect post-PNX lung growth.…”

Section: Discussionmentioning

confidence: 99%

Twist1 signaling in age-dependent decline in angiogenesis and lung regeneration

Hendee

Hunyenyiwa

Matus

et al. 2021

Aging

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Angiogenesis – the formation of new blood capillaries- is impaired in aging animals and contributes to the pathogenesis of age-related diseases. A transcription factor, Twist1, contributes to the pathogenesis of age- and angiogenesis-related diseases such as pulmonary fibrosis and atherosclerosis. However, the mechanism by which Twist1 controls age-dependent decline in angiogenesis remains unclear. In this report, we have demonstrated that the levels of Twist1 are higher, while the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) that stimulates angiogenesis, is lower in endothelial cells (ECs) isolated from aged human adipose tissues and mouse lungs compared to those from young tissues. Knockdown of Twist1 in aged human ECs increases the levels of PGC1α and angiogenic factor receptor, vascular endothelial growth factor receptor (VEGFR2), and restores EC proliferation and migration, while inhibition of PGC1α suppresses these effects. Knockdown of Twist1 in supplemented aged ECs also restores vascular networks in the subcutaneously implanted gel, while these effects are abrogated by knockdown of PGC1α. Age-dependent inhibition of post-pneumonectomy (PNX) lung growth is suppressed in Tie2-specific Twist1 conditional knockout mouse lungs, in which VEGFR2 expression increases after PNX. These results suggest that upregulation of endothelial Twist1 mediates age-dependent decline in angiogenesis and regenerative lung growth.

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Section: Discussionmentioning

confidence: 99%

Twist1 signaling in age-dependent decline in angiogenesis and lung regeneration

Hendee

Hunyenyiwa

Matus

et al. 2021

Aging

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“…The pulmonary capillary microvascular niche in lungs supports alveolar epithelial repair mechanisms following injury, e.g. by secretion of MMP14, VEGF, thrombospondin-1 (THBS1) (Mammoto and Mammoto, 2019). Analysis of pulmonary endothelial cell subclusters revealed that bronchial, pulmonary capillary and pulmonary vein endothelial cells showed increased expression of Thbs1 at 5, but not 14 dpi.…”

Section: Discussionmentioning

confidence: 99%

Longitudinal omics in Syrian hamsters integrated with human data unravel complexity of moderate immune responses to SARS-CoV-2

Nouailles

Wyler

Pennitz

et al. 2020

Preprint

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In COVID-19, the immune response largely determines disease severity and is key to therapeutic strategies. Cellular mechanisms contributing to inflammatory lung injury and tissue repair in SARS-CoV-2 infection, particularly endothelial cell involvement, remain ill-defined. We performed detailed spatiotemporal analyses of cellular and molecular processes in SARS-CoV-2 infected Syrian hamsters. Comparison of hamster single-cell sequencing and proteomics with data sets from COVID-19 patients demonstrated inter-species concordance of cellular and molecular host-pathogen interactions. In depth vascular and pulmonary compartment analyses (i) supported the hypothesis that monocyte-derived macrophages dominate inflammation, (ii) revealed endothelial inflammation status and T-cell attraction, and (iii) showed that CD4+ and CD8+ cytotoxic T-cell responses precede viral elimination. Using the Syrian hamster model of self-limited moderate COVID-19, we defined the specific roles of endothelial and epithelial cells, among other myeloid and non-myeloid lung cell subtypes, for determining the disease course.

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“…Human lung development can be histologically divided into four distinguishable stages: embryonic and pseudoglandular stages (human, week 4–17 and mouse, E9.5–E16.5), canalicular stage (human, week 17–26 and mouse, E16.5–E17.5), saccular stage (human, week 26–36 and mouse, E17.5–PN5), and alveolar stage (human, week 36–8 years and mouse, PN5–PN30) [ 46 , 47 ].…”

Section: Development Of Normal Pulmonary Vasculature and Bpd-ph Frmentioning

confidence: 99%

“…From E11 to E12, proximal vessels sprout from the main pulmonary trunk (proximal angiogenesis), run along the main conducting airways, as well as its many ramified branches. In addition, the distal blood islands increase markedly and are connected together to form the primitive capillary plexus (distal angiogenesis) [ 46 ]. During the late pseudoglandular stage, the capillary network, around lung buds, fuses with the proximal vessels.…”

Section: Development Of Normal Pulmonary Vasculature and Bpd-ph Frmentioning

confidence: 99%

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

Chao

Lei

Chu

et al. 2020

Cells

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More than 50 years after the first description of Bronchopulmonary dysplasia (BPD) by Northway, this chronic lung disease affecting many preterm infants is still poorly understood. Additonally, approximately 40% of preterm infants suffering from severe BPD also suffer from Bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH), leading to a significant increase in total morbidity and mortality. Until today, there is no curative therapy for both BPD and BPD-PH available. It has become increasingly evident that growth factors are playing a central role in normal and pathologic development of the pulmonary vasculature. Thus, this review aims to summarize the recent evidence in our understanding of BPD-PH from a basic scientific point of view, focusing on the potential role of Fibroblast Growth Factor (FGF)/FGF10 signaling pathway contributing to disease development, progression and resolution.

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Vascular Niche in Lung Alveolar Development, Homeostasis, and Regeneration

Cited by 56 publications

References 186 publications

Twist1 signaling in age-dependent decline in angiogenesis and lung regeneration

Twist1 signaling in age-dependent decline in angiogenesis and lung regeneration

Longitudinal omics in Syrian hamsters integrated with human data unravel complexity of moderate immune responses to SARS-CoV-2

Targeting Bronchopulmonary Dysplasia-Associated Pulmonary Hypertension (BPD-PH): Potential Role of the FGF Signaling Pathway in the Development of the Pulmonary Vascular System

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