ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018
Developmental differences in focal adhesion kinase expression modulate pulmonary endothelial barrier function in response to inflammation.
Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Long-Term Consequences of Asymptomatic SARS-CoV-2 Infection: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2023Pooled it
- From development to regeneration: the endothelial interface in lung injury and repair.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Yes-associated protein induces age-dependent inflammatory signaling in the pulmonary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Integrated bioinformatics analysis screened the key genes and pathways of idiopathic pulmonary fibrosis.Scientific reports · 2025Article
- Precision Medicine for Pulmonary Vascular Disease: The Future Is Now (2023 Grover Conference Series).Pulmonary circulation · 2025Article
- FAK regulates tension transmission to the nucleus and endothelial transcriptome independent of kinase activity.Cell reports · 2024Article
- COVID-19 Disease in Under-5 Children: Current Status and Strategies for Prevention including Vaccination.Vaccines · 2023Review
- Dam-Infant Rhesus Macaque Pairs to Dissect Age-Dependent Responses to SARS-CoV-2 Infection.ImmunoHorizons · 2022Article
- Adenovirus type 5 SARS-CoV-2 vaccines delivered orally or intranasally reduced disease severity and transmission in a hamster model.Science translational medicine · 2022Article
- Angiopoietin-1 protects against endotoxin-induced neonatal lung injury and alveolar simplification in mice.Pediatric research · 2022Article
- The Protective Effect of Artesunate on LPS-Induced Acute Respiratory Distress Syndrome through Inhibiting NLRP3 Inflammasome Signaling.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Lipocalin-2 silencing suppresses inflammation and oxidative stress of acute respiratory distress syndrome by ferroptosis via inhibition of MAPK/ERK pathway in neonatal mice.Bioengineered · 2022Article
- Influence of Fucoidan Extracts from Different Fucus Species on Adult Stem Cells and Molecular Mediators in In Vitro Models for Bone Formation and Vascularization.Marine drugs · 2021Article
- Understanding the age divide in COVID-19: why are children overwhelmingly spared?American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Ibudilast, a Phosphodiesterase-4 Inhibitor, Ameliorates Acute Respiratory Distress Syndrome in Neonatal Mice by Alleviating Inflammation and Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Interleukin-37 Attenuates Lipopolysaccharide (LPS)-Induced Neonatal Acute Respiratory Distress Syndrome in Young Mice via Inhibition of Inflammation and Cell Apoptosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Cortical Actin Dynamics in Endothelial Permeability.Current topics in membranes · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Compromised pulmonary endothelial cell (PEC) barrier function characterizes acute respiratory distress syndrome (ARDS), a cause of substantial morbidity and mortality. Survival from ARDS is greater in children compared with adults. Whether developmental differences intrinsic to PEC barrier function contribute to this survival advantage remains unknown. To test the hypothesis that PEC barrier function is more well-preserved in neonatal lungs compared with adult lungs in response to inflammation, we induced lung injury in neonatal and adult mice with systemic lipopolysaccharide (LPS). We assessed PEC barrier function in vivo and in vitro, evaluated changes in the expression of focal adhesion kinase 1 (FAK1) and phosphorylation in response to LPS, and determined the effect of FAK silencing and overexpression on PEC barrier function. We found that LPS induced a greater increase in lung permeability and PEC barrier disruption in the adult mice, despite similar degrees of inflammation and apoptosis. Although baseline expression was similar, LPS increased FAK1 expression in neonatal PEC but increased FAK1 phosphorylation and decreased FAK1 expression in adult PEC. Pharmacologic inhibition of FAK1 accentuated LPS-induced barrier disruption most in adult PEC. Finally, in response to LPS, FAK silencing markedly impaired neonatal PEC barrier function, whereas FAK overexpression preserved adult PEC barrier function. Thus, developmental differences in FAK expression during inflammatory injury serve to preserve neonatal pulmonary endothelial barrier function compared with that of adults and suggest that intrinsic differences in the immature versus pulmonary endothelium, especially relative to FAK1 phosphorylation, may contribute to the improved outcomes of children with ARDS.
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