ArticleMolecular biology of the cell2005
Cytosolic phospholipase A2-alpha mediates endothelial cell proliferation and is inactivated by association with the Golgi apparatus.
Article in Molecular biology of the cell, 2005. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Mechanotransduction by nuclear envelope tension.Nucleus (Austin, Tex.) · 2026Review
- Elevated hydrostatic pressure destabilizes VE-cadherin junctions in a time and shear stress dependent manner: An endothelium-on-chip study.APL bioengineering · 2025Article
- Phospholipase Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021Review
- C2 domain membrane penetration by group IVA cytosolic phospholipase A₂ induces membrane curvature changes.Journal of lipid research · 2012Article
- 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 PLA1-2 punch regulates the Golgi complex.Trends in cell biology · 2012Review
- Phospholipase A2 enzymes: physical structure, biological function, disease implication, chemical inhibition, and therapeutic intervention.Chemical reviews · 2011Review
- GVI phospholipase A2 role in the stimulatory effect of sphingosine-1-phosphate on TRPC5 cationic channels.Cell calcium · 2011Article
- Attachment of HeLa cells during early G1 phase.Histochemistry and cell biology · 2011Article
- Review
- Cytosolic phospholipase A2 activation correlates with HER2 overexpression and mediates estrogen-dependent breast cancer cell growth.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Novel role of cPLA(2)alpha in membrane and actin dynamics.Cellular and molecular life sciences : CMLS · 2010Article
- Golgi-associated cPLA2alpha regulates endothelial cell-cell junction integrity by controlling the trafficking of transmembrane junction proteins.Molecular biology of the cell · 2009Article
- Rab GTPase regulation of VEGFR2 trafficking and signaling in endothelial cells.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- Activation of cytosolic phospholipase A2-{alpha} as a novel mechanism regulating endothelial cell cycle progression and angiogenesis.The Journal of biological chemistry · 2009Article
- Regulation of Wnt/beta-catenin pathway by cPLA2alpha and PPARdelta.Journal of cellular biochemistry · 2008Article
- iPLA2beta: front and center in human monocyte chemotaxis to MCP-1.The Journal of experimental medicine · 2008Article
- Roles of cPLA2alpha and arachidonic acid in cancer.Biochimica et biophysica acta · 2006Review
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.
Funding
Abstract
Arachidonic acid and its metabolites are implicated in regulating endothelial cell proliferation. Cytosolic phospholipase A2-alpha (cPLA2alpha) is responsible for receptor-mediated arachidonic acid evolution. We tested the hypothesis that cPLA2alpha activity is linked to endothelial cell proliferation. The specific cPLA2alpha inhibitor, pyrrolidine-1, inhibited umbilical vein endothelial cell (HUVEC) proliferation in a dose-dependent manner. Exogenous arachidonic acid addition reversed this inhibitory effect. Inhibition of sPLA2 did not affect HUVEC proliferation. The levels of cPLA2alpha did not differ between subconfluent and confluent cultures of cells. However, using fluorescence microscopy we observed a novel, confluence-dependent redistribution of cPLA2alpha to the distal Golgi apparatus in HUVECs. Association of cPLA2alpha with the Golgi was linked to the proliferative status of HUVECs. When associated with the Golgi apparatus, cPLA2alpha activity was seen to be 87% inhibited. Relocation of cPLA2alpha to the cytoplasm and nucleus, and cPLA2alpha enzyme activity were required for cell cycle entry upon mechanical wounding of confluent monolayers. Thus, cPLA2alpha activity and function in controlling endothelial cell proliferation is regulated by reversible association with the Golgi apparatus.
Indexed as
Identifiers
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.