ArticleThe Journal of biological chemistry2009
Activation of cytosolic phospholipase A2-{alpha} as a novel mechanism regulating endothelial cell cycle progression and angiogenesis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 37 citations in OpenAlex.
- Therapeutic targeting of protein arginine methyltransferases reduces breast cancer progression by disrupting angiogenic pathways.Biochemistry and biophysics reports · 2025Review
- Acute partial sleep restriction does not impact arterial function in young and healthy humans.Experimental physiology · 2024Article
- Targeting the eicosanoid pathway in hepatocellular carcinoma.American journal of cancer research · 2021Review
- Phospholipase Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Review
- Focus on the glycerophosphocholine pathway in choline phospholipid metabolism of cancer.NMR in biomedicine · 2019Review
- Emerging role of 12/15-Lipoxygenase (ALOX15) in human pathologies.Progress in lipid research · 2019Review
- cPLA2α mediates TGF-β-induced epithelial-mesenchymal transition in breast cancer through PI3k/Akt signaling.Cell death & disease · 2017Article
- Cytosolic phospholipaseA2 inhibition with PLA-695 radiosensitizes tumors in lung cancer animal models.PloS one · 2013Article
- Phospholipase signalling networks in cancer.Nature reviews. Cancer · 2012Review
- A VE-cadherin-PAR3-α-catenin complex regulates the Golgi localization and activity of cytosolic phospholipase A(2)α in endothelial cells.Molecular biology of the cell · 2012Article
- A heat-shock protein axis regulates VEGFR2 proteolysis, blood vessel development and repair.PloS one · 2012Article
- Dre-miR-2188 targets Nrp2a and mediates proper intersegmental vessel development in zebrafish embryos.PloS one · 2012Article
- Article
- GVI phospholipase A2 role in the stimulatory effect of sphingosine-1-phosphate on TRPC5 cationic channels.Cell calcium · 2011Article
- Activation of cytosolic phospholipase A2 downstream of the Src-phospholipase D1 (PLD1)-protein kinase C γ (PKCγ) signaling axis is required for hypoxia-induced pathological retinal angiogenesis.The Journal of biological chemistry · 2011Article
- Towards novel radiosensitizing agents: the role of cytosolic PLA2α in combined modality cancer therapy.Future medicinal chemistry · 2011Review
- Article
- Cytosolic phospholipase A2 and lysophospholipids in tumor angiogenesis.Journal of the National Cancer Institute · 2010Article
- Membrane phospholipids, EML4-ALK, and Hsp90 as novel targets in lung cancer treatment.Cancer journal (Sudbury, Mass.)Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Release of endothelial cells from contact-inhibition and cell cycle re-entry is required for the induction of new blood vessel formation by angiogenesis. Using a combination of chemical inhibition, loss of function, and gain of function approaches, we demonstrate that endothelial cell cycle re-entry, S phase progression, and subsequent angiogenic tubule formation are dependent upon the activity of cytosolic phospholipase A(2)-alpha (cPLA(2)alpha). Inhibition of cPLA(2)alpha activity and small interfering RNA (siRNA)-mediated knockdown of endogenous cPLA(2)alpha reduced endothelial cell proliferation. In the absence of cPLA(2)alpha activity, endothelial cells exhibited retarded progression from G(1) through S phase, displayed reduced cyclin A/cdk2 expression, and generated less arachidonic acid. In quiescent endothelial cells, cPLA(2)alpha is inactivated upon its sequestration at the Golgi apparatus. Upon the stimulation of endothelial cell proliferation, activation of cPLA(2)alpha by release from the Golgi apparatus was critical to the induction of cyclin A expression and efficient cell cycle progression. Consequently, inhibition of cPLA(2)alpha was sufficient to block angiogenic tubule formation in vitro. Furthermore, the siRNA-mediated retardation of endothelial cell cycle re-entry and proliferation was reversed upon overexpression of an siRNA-resistant form of cPLA(2)alpha. Thus, activation of cPLA(2)alpha acts as a novel mechanism for the regulation of endothelial cell cycle re-entry, cell cycle progression, and angiogenesis.
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What OpenQuestion holds
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.