ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Leukocyte-endothelial cell interactions are linked to vascular permeability via ICAM-1-mediated signaling.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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75 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Pooled it
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- Mechanisms That Prevent Vascular Leakage During Leukocyte Extravasation.Acta physiologica (Oxford, England) · 2025Review
- HuR-Regulated Extracellular Vesicles Promote Endothelial Cell Remodeling in Pancreatic Cancer.Cancer research communications · 2025Article
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- A High-Fat Diet Induces Low-Grade Cochlear Inflammation in CD-1 Mice.International journal of molecular sciences · 2022Article
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15 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
Two key characteristics of the inflammatory response are the recruitment of leukocytes to inflamed tissue as well as changes in vessel permeability. We explored the relationship between these two processes using intravital confocal microscopy in cremasters of anesthetized (65 mg/kg Nembutal ip) mice. We provide direct evidence that intercellular adhesion molecule-1 (ICAM-1) links leukocyte-endothelial cell interactions and changes in solute permeability (Ps). Importantly, we show that arterioles, not just venules, respond to proinflammatory stimuli, thus contributing to microvascular exchange. We identified two independent, ICAM-1-mediated pathways regulating Ps. Under control conditions in wild-type (WT) mice, there is a constitutive PKC-dependent pathway (Ps = 1.0 +/- 0.10 and 2.2 +/- 0.46 x 10(-6) cm/s in arterioles and venules, respectively), which was significantly reduced in ICAM-1 knockout (KO) mice (Ps = 0.54 +/- 0.07 and 0.77 +/- 0.11 x 10(-6) cm/s). The PKC inhibitor bisindolylmaleimid l (1 micromol/l in 0.01% DMSO) decreased P(s) in WT mice to levels similar to those in ICAM-1 KO mice. Likewise, a PKC activator (phorbol-12-myristate-acetate; 1 micromol/l in 0.01% DMSO) successfully restored Ps in ICAM-1 KO vessels to be not different from that of the WT controls. On the other hand, during TNF-alpha-induced inflammation, Ps in WT mice was significantly increased (2-fold in venules and 2.5-fold in arterioles) in a Src-dependent and PKC-independent manner. The blockade of Src (PP2; 2 micromol/l in 0.01% DMSO) but not PKC significantly reduced the TNF-alpha-dependent increase in Ps. We conclude that ICAM-1 plays an essential role in the regulation of Ps in microvessels and that there are two separate (constitutive and inducible) signaling pathways that regulate permeability under normal and inflamed conditions.
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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.