ArticleJournal of immunology (Baltimore, Md. : 1950)2006
VCAM-1 signals activate endothelial cell protein kinase Calpha via oxidation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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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.
The trial behind it
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
41 citing papers in PubMed, 72 citations in OpenAlex.
- Assessing the therapeutic potential of a panel of novel VCAM-1 antibodies using microfluidic and three-dimensionalAntibody therapeutics · 2025Article
- Maternal supplementation with α-tocopherol inhibits the development of offspring food allergy, H1R signaling and ultimately anaphylaxis early in life.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- 5-HTP inhibits eosinophilia via intracellular endothelial 5-HTRs; SNPs in 5-HTRs associate with asthmatic lung function.Frontiers in allergy · 2024Article
- Targeting endothelial vascular cell adhesion molecule-1 in atherosclerosis: drug discovery and development of vascular cell adhesion molecule-1-directed novel therapeutics.Cardiovascular research · 2023Review
- Dysbiotic lung microbial communities of neonates from allergic mothers confer neonate responsiveness to suboptimal allergen.Frontiers in allergy · 2023Article
- Asthma, allergy and vitamin E: Current and future perspectives.Free radical biology & medicine · 2022Article
- VCAM-1 induces signals that stimulate ZO-1 serine phosphorylation and reduces ZO-1 localization at lung endothelial cell junctions.Journal of leukocyte biology · 2018Article
- Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease.Biochemical pharmacology · 2018Review
- Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Oxidative Stress: Harms and Benefits for Human Health.Oxidative medicine and cellular longevity · 2017Review
- Article
- Regulation of allergic lung inflammation by endothelial cell transglutaminase 2.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Crossing the Vascular Wall: Common and Unique Mechanisms Exploited by Different Leukocyte Subsets during Extravasation.Mediators of inflammation · 2015Review
- Vitamin E isoforms as modulators of lung inflammation.Nutrients · 2013Review
- Redox signaling in cardiovascular health and disease.Free radical biology & medicine · 2013Review
- Isoforms of Vitamin E Differentially Regulate PKCJournal of clinical & cellular immunology · 2013Article
- Endothelial cell PTP1B regulates leukocyte recruitment during allergic inflammation.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Getting leukocytes to the site of inflammation.Veterinary pathology · 2013Review
- Article
- Inhibition of allergic inflammation by supplementation with 5-hydroxytryptophan.American journal of physiology. Lung cellular and molecular physiology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lymphocyte binding to VCAM-1 activates endothelial cell NADPH oxidase, resulting in the generation of 1 muM H(2)O(2). This is required for VCAM-1-dependent lymphocyte migration. In this study, we identified a role for protein kinase Calpha (PKCalpha) in VCAM-1 signal transduction in human and mouse endothelial cells. VCAM-1-dependent spleen cell migration under 2 dynes/cm(2) laminar flow was blocked by pretreatment of endothelial cells with dominant-negative PKCalpha or the PKCalpha inhibitors, Rö-32-0432 or Gö-6976. Phosphorylation of PKCalpha(Thr638), an autophosphorylation site indicating enzyme activity, was increased by Ab cross-linking of VCAM-1 on endothelial cells or by the exogenous addition of 1 muM H(2)O(2). The anti-VCAM-1-stimulated phosphorylation of PKCalpha(Thr638) was blocked by scavenging of H(2)O(2) and by inhibition of NADPH oxidase. Furthermore, anti-VCAM-1 signaling induced the oxidation of endothelial cell PKCalpha. Oxidized PKCalpha is a transiently active form of PKCalpha that is diacylglycerol independent. This oxidation was blocked by inhibition of NADPH oxidase. In summary, VCAM-1 activation of endothelial cell NADPH oxidase induces transient PKCalpha activation that is necessary for VCAM-1-dependent transendothelial cell migration.
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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.