ArticlePlacenta2009
Suppression of protein phosphatase 2 differentially modulates VEGF- and FGF2-induced signaling in ovine fetoplacental artery endothelial cells.
Article in Placenta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 10 citations in OpenAlex.
- An endogenous aryl hydrocarbon receptor ligand dysregulates endothelial functions, transcriptome, and phosphoproteome.American journal of physiology. Cell physiology · 2025Article
- Genome-wide association analysis reveals the genetic locus for high reproduction trait in Chinese Arbas Cashmere goat.Genes & genomics · 2020Article
- Selection signatures of litter size in Dazu black goats based on a whole genome sequencing mixed pools strategy.Molecular biology reports · 2019Article
- GNA11 differentially mediates fibroblast growth factor 2- and vascular endothelial growth factor A-induced cellular responses in human fetoplacental endothelial cells.The Journal of physiology · 2018Article
- Smad4-dependent suppressor pituitary homeobox 2 promotes PPP2R2A-mediated inhibition of Akt pathway in pancreatic cancer.Oncotarget · 2016Article
- An endogenous aryl hydrocarbon receptor ligand inhibits proliferation and migration of human ovarian cancer cells.Cancer letters · 2013Article
- Signaling regulation of fetoplacental angiogenesis.The Journal of endocrinology · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2) elicit cellular responses via activation of protein kinases and phosphatases. We have reported that the MEK1/2/ERK1/2 and PI3K/AKT1 pathways are critical for VEGF- and FGF2-stimulated ovine fetoplacental artery endothelial (OFPAE) cell proliferation. We have also shown that protein phosphatase 3 (PPP3) differentially modulates VEGF- and FGF2-stimulated cell proliferation and activation of ERK1/2 and AKT1 in OFPAE cells. Herein, we investigated if protein phosphatase 2 (PPP2) modulated VEGF- and FGF2-induced ERK1/2, AKT1, and p38 MAPK activation and VEGF- and FGF2-stimulated cell proliferation in OFPAE cells. Small interfering RNA (siRNA) specifically targeting human PPP2CA catalytic subunit alpha (PPP2CA) was used to suppress PPP2CA expression in OFPAE cells. When compared with scrambled siRNA, PPP2CA siRNA decreased (p<0.05) PPP2CA protein levels (approximately 70%) and activity (approximately 50%) without altering protein levels of PPP3 catalytic subunit alpha (PPP3CA), nitric oxide synthase 3 (NOS3), ERK1/2, AKT1, and p38 MAPK. FGF2, but not VEGF rapidly (< or =5 min) induced p38 MAPK phosphorylation. Suppression of PPP2CA enhanced (p<0.05) VEGF-induced AKT1, but not ERK1/2 phosphorylation, whereas inhibited (p<0.05) FGF2-induced ERK1/2 and p38 MAPK and slightly attenuated FGF2-induced AKT1 phosphorylation. Suppression of PPP2CA did not significantly affect VEGF- and FGF2-stimulated OFPAE cell proliferation. Thus, suppression of PPP2CA alone differentially modulated VEGF- and FGF2-induced ERK1/2, AKT1, and p38 MAPK activation, without altering VEGF- and FGF2-stimulated cell proliferation in OFPAE cells. These data also suggest that signaling molecules other than ERK1/2, AKT1, and p38 MAPK are important mediators for VEGF- and FGF2-stimulated OFPAE cell proliferation after PPP2CA suppression.
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