ArticleThe American journal of pathology2009
Sphingosine kinase-1 associates with integrin {alpha}V{beta}3 to mediate endothelial cell survival.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 18 citations in OpenAlex.
- A Rheostat of Ceramide and Sphingosine-1-Phosphate as a Determinant of Oxidative Stress-Mediated Kidney Injury.International journal of molecular sciences · 2022Review
- Understanding the role of integrins in breast cancer invasion, metastasis, angiogenesis, and drug resistance.Oncogene · 2021Review
- Molecular mechanisms of regulation of sphingosine kinase 1.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Review
- Sphingolipids in spinal cord injury.International journal of physiology, pathophysiology and pharmacology · 2016Review
- Sphingosine 1-phosphate is a ligand for peroxisome proliferator-activated receptor-γ that regulates neoangiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Dengue Virus-Induced Inflammation of the Endothelium and the Potential Roles of Sphingosine Kinase-1 and MicroRNAs.Mediators of inflammation · 2015Review
- Sphingolipids: a potential molecular approach to treat allergic inflammation.Journal of allergy · 2012Article
- Tumor necrosis factor-induced neutrophil adhesion occurs via sphingosine kinase-1-dependent activation of endothelial {alpha}5{beta}1 integrin.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingosine kinase (SK)-1 promotes endothelial cell (EC) survival through the cell junction molecule CD31 (platelet endothelial cell adhesion molecule-1). The integrin alpha(v)beta(3) is also essential for EC survival; inhibition of alpha(v)beta(3) ligation promotes apoptosis. Herein we demonstrate that under basal conditions, SK-1, alpha(v)beta(3), and CD31 exist as a heterotrimeric complex. Under conditions that affect EC survival such as loss of contact with the extracellular matrix or growth factor activation, more of this heterotrimeric complex forms. Overexpression studies demonstrate a requirement for SK-1 phosphorylation at serine 225 for increased heterotrimeric complex formation, activation of alpha(v)beta(3), and EC survival signals, including Bcl-X and nuclear factor-kappaB pathways. Moreover, beta(3) integrin depletion confirmed the requirement for this heterotrimeric complex in SK-1-mediated EC survival. Thus, with alpha(v)beta(3) integrin being identifiable primarily on angiogenic ECs and SK-1 being highly expressed in tumors, targeting SK-1 may affect multiple survival pathways, and its inhibition may be highly efficacious in controlling pathological EC survival.
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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.