ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Characterization of TNF receptor subtype expression and signaling on pulmonary endothelial cells in mice.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Inflammation and Immune Dysregulation Across Respiratory Diseases: From Cellular Mechanisms to Therapeutic Targets.Journal of inflammation research · 2026Review
- Hepatic conditioning results in better lung endothelial cell preservation under hypoxic environment in vitro.The International journal of artificial organs · 2025Article
- Comprehensive overview of COVID-19-related respiratory failure: focus on cellular interactions.Cellular & molecular biology letters · 2022Review
- Dichotomous Role of Tumor Necrosis Factor in Pulmonary Barrier Function and Alveolar Fluid Clearance.Frontiers in physiology · 2021Review
- TNFR2: Role in Cancer Immunology and Immunotherapy.ImmunoTargets and therapy · 2021Review
- Blueberry-Derived Exosome-Like Nanoparticles Counter the Response to TNF-α-Induced Change on Gene Expression in EA.hy926 Cells.Biomolecules · 2020Article
- Ventilation following established ARDS: a preclinical model framework to improve predictive power.Thorax · 2019Article
- Article
- Kinetic profiling of in vivo lung cellular inflammatory responses to mechanical ventilation.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Article
- Release of nonmuscle myosin II from the cytosolic domain of tumor necrosis factor receptor 2 is required for target gene expression.Science signaling · 2013Article
- TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Expression, regulation, and function of atypical chemerin receptor CCRL2 on endothelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Regulation of monocyte subset proinflammatory responses within the lung microvasculature by the p38 MAPK/MK2 pathway.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
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Authors and funding
7 authors.
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Abstract
TNF plays a crucial role in the pathogenesis of acute lung injury. However, the expression profile of its two receptors, p55 and p75, on pulmonary endothelium and their influence on TNF signaling during lung microvascular inflammation remain uncertain. Using flow cytometry, we characterized the expression profile of TNF receptors on the surface of freshly harvested pulmonary endothelial cells (PECs) from mice and found expression of both receptors with dominance of p55. To investigate the impact of stimulating individual TNF receptors, we treated wild-type and TNF receptor knockout mice with intravenous TNF and determined surface expression of adhesion molecules (E-selectin, VCAM-1, ICAM-1) on PECs by flow cytometry. TNF-induced upregulation of all adhesion molecules was substantially attenuated by absence of p55, whereas lack of p75 had a similar but smaller effect that varied between adhesion molecules. Selective blockade of individual TNF receptors by specific antibodies in wild-type primary PEC culture confirmed that the in vivo findings were due to direct effects of TNF receptor inhibition on endothelium and not other cells (e.g., circulating leukocytes). Finally, we found that PEC surface expression of p55 dramatically decreased in the early stages of endotoxemia following intravenous LPS, while no change in p75 expression was detected. These data demonstrate a crucial in vivo role of p55 and an auxiliary role of p75 in TNF-mediated adhesion molecule upregulation on PECs. It is possible that the importance of the individual receptors varies at different stages of pulmonary microvascular inflammation following changes in their relative expression.
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