ArticleThe Journal of clinical investigation1997
Barrier effects of hyperosmolar signaling in microvascular endothelium of rat lung.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Microvascular fluid flow in ex vivo and engineered lungs.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Hypertonic stress modulates eNOS function through O-GlcNAc modification at Thr-866.Scientific reports · 2021Article
- Functional vascularized lung grafts for lung bioengineering.Science advances · 2017Article
- Role played by paxillin and paxillin tyrosine phosphorylation in hepatocyte growth factor/sphingosine-1-phosphate-mediated reactive oxygen species generation, lamellipodia formation, and endothelial barrier function.Pulmonary circulation · 2015Article
- Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Article
- Protective effects of high-molecular weight polyethylene glycol (PEG) in human lung endothelial cell barrier regulation: role of actin cytoskeletal rearrangement.Microvascular research · 2009Article
- Chloride-dependent secretion of alveolar wall liquid determined by optical-sectioning microscopy.American journal of respiratory cell and molecular biology · 2007Article
- Hyperosmolarity enhances the lung capillary barrier.The Journal of clinical investigation · 2003Article
- Hyperosmotically induced volume change and calcium signaling in intervertebral disk cells: the role of the actin cytoskeleton.Biophysical journal · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We determined the effects of hyperosmolarity on lung microvascular barrier properties by means of the split-drop technique in single venular capillaries of the isolated, blood-perfused rat lung. Using isosmolar and hyperosmolar test solutions (colloid osmotic pressure = 21 cm H2O), we quantified transcapillary flux at a fixed absorptive capillary pressure, and the capillary hydraulic conductivity (Lp). Loss of barrier function was indicated in flux reversal from isosmolar absorption to hyperosmolar filtration (P < 0. 01), and by hyperosmolarity-induced Lp increase (P < 0.01). Barrier recovery after a 1-min hyperosmolar exposure was delayed > 25 min. The flux reversal was blocked by the tyrosine kinase inhibitors genistein and MDC (P < 0.01). Genistein also inhibited the Lp increase (P < 0.01). Immunoblots of hyperosmolarity-exposed, cultured rat lung microvascular endothelial cells (RLMEC) and of endothelial cells freshly harvested from lungs given hyperosmolar infusions indicated a genistein-inhibitable enhancement of protein tyrosine phosphorylation. Immunoprecipitation studies indicated tyrosine phosphorylation of the mitogen activated protein kinases (MAPK) ERK1 and ERK2 and the adaptor protein Shc in lysates of RLMEC exposed to hyperosmolar conditions. We conclude that in lung venular capillaries hyperosmolarity deteriorates barrier properties, possibly by inducing tyrosine phosphorylation of endothelial proteins.
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