ArticleThe Journal of clinical investigation2000
A novel signaling mechanism between gas and blood compartments of the lung.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 110 citations in OpenAlex.
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- Mitochondria and their potential role in acute lung injury (Review).Experimental and therapeutic medicine · 2022Review
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- Current Challenges for the Effective Management of the COVID-19 Pandemic.Advances in experimental medicine and biology · 2021Article
- A perpetual switching system in pulmonary capillaries.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Article
- Using cultured endothelial cells to study endothelial barrier dysfunction: Challenges and opportunities.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Macrophage-epithelial interactions in pulmonary alveoli.Seminars in immunopathology · 2016Review
- Multidimensional immunolabeling and 4D time-lapse imaging of vital ex vivo lung tissue.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Hypercapnia attenuates ventilator-induced lung injury via a disintegrin and metalloprotease-17.The Journal of physiology · 2014Article
- Quantifying single microvessel permeability in isolated blood-perfused rat lung preparation.Journal of visualized experiments : JoVE · 2014Article
- Sessile alveolar macrophages communicate with alveolar epithelium to modulate immunity.Nature · 2014Article
- Live imaging of the lung.Annual review of physiology · 2014Review
- Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction.The Journal of clinical investigation · 2012Article
- Endothelial connexin43 mediates acid-induced increases in pulmonary microvascular permeability.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Localized acid instillation by a wedged-catheter method reveals a role for vascular gap junctions in spatial expansion of acid injury.Anatomical record (Hoboken, N.J. : 2007) · 2011Article
- Spontaneous lung dysfunction and fibrosis in mice lacking connexin 40 and endothelial cell connexin 43.The American journal of pathology · 2011Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Propagation of inflammatory signals from the airspace to the vascular space is pivotal in lung inflammation, but mechanisms of intercompartmental signaling are not understood. To define signaling mechanisms, we microinfused single alveoli of blood-perfused rat lung with TNF-alpha, and determined in situ cytosolic Ca(2+) concentration ([Ca(2+)](i)) by the fura-2 ratio method, cytosolic phospholipase A(2) (cPLA(2)) activation and P-selectin expression by indirect immunofluorescence. Alveolar TNF-alpha increased [Ca(2+)](i) and activated cPLA(2) in alveolar epithelial cells, and increased both endothelial [Ca(2+)](i) and P-selectin expression in adjoining perialveolar capillaries. All responses were blocked by pretreating alveoli with a mAb against TNF receptor 1 (TNFR1). Crosslinking alveolar TNFR1 also increased endothelial [Ca(2+)](i). However, the endothelial responses to alveolar TNF-alpha were blocked by alveolar preinjection of the intracellular Ca(2+) chelator BAPTA-AM, or the cPLA(2) blockers AACOCF(3) and MAFP. The gap-junction uncoupler heptanol had no effect. We conclude that TNF-alpha induces signaling between the alveolar and vascular compartments of the lung. The signaling is attributable to ligation of alveolar TNFR1 followed by receptor-mediated [Ca(2+)](i) increases and cPLA(2) activation in alveolar epithelium. These novel mechanisms may be relevant in the alveolar recruitment of leukocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.