ArticlePloS one2011
Prostaglandin E2 promotes endothelial differentiation from bone marrow-derived cells through AMPK activation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 53 citations in OpenAlex.
- Lipid Metabolism in Gastrointestinal Malignancies: Exploring Dysregulation, Biomarkers, and Treatment Strategies.Cancer medicine · 2025Review
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- Evaluation of the Antioxidant and Antiangiogenic Activity of a Pomegranate Extract in BPH-1 Prostate Epithelial Cells.International journal of molecular sciences · 2023Article
- Improved osteogenic differentiation by extremely low electromagnetic field exposure: possible application for bone engineering.Histochemistry and cell biology · 2022Article
- Immune Function of Endothelial Cells: Evolutionary Aspects, Molecular Biology and Role in Atherogenesis.International journal of molecular sciences · 2022Review
- Notch-activated mesenchymal stromal/stem cells enhance the protective effect against acetaminophen-induced acute liver injury by activating AMPK/SIRT1 pathway.Stem cell research & therapy · 2022Article
- The sustained PGEJournal of nanobiotechnology · 2022Article
- Salvianolic Acid B Suppresses ER Stress-Induced NLRP3 Inflammasome and Pyroptosis via the AMPK/FoxO4 and Syndecan-4/Rac1 Signaling Pathways in Human Endothelial Progenitor Cells.Oxidative medicine and cellular longevity · 2022Article
- Endothelial cell prostaglandin E2 receptor EP4 is essential for blood pressure homeostasis.JCI insight · 2020Article
- Review
- Aspirin Suppresses PGECancer prevention research (Philadelphia, Pa.) · 2018Article
- Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated Protein Kinases (ERK) Signaling Pathway.International journal of molecular sciences · 2018Article
- Inositol Polyphosphate Multikinase Inhibits Angiogenesis via Inositol Pentakisphosphate-Induced HIF-1α Degradation.Circulation research · 2018Article
- Neuronal migration is mediated by inositol hexakisphosphate kinase 1 via α-actinin and focal adhesion kinase.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Possible involvement of AMP-activated protein kinase in PGEExperimental and therapeutic medicine · 2016Article
- Doxorubicin resistant cancer cells activate myeloid-derived suppressor cells by releasing PGE2.Scientific reports · 2016Article
- Prostaglandin E2/cyclooxygenase pathway in human skeletal muscle: influence of muscle fiber type and age.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Inositol Hexakisphosphate Kinase-3 Regulates the Morphology and Synapse Formation of Cerebellar Purkinje Cells via Spectrin/Adducin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Angiogenesis in the primate ovulatory follicle is stimulated by luteinizing hormone via prostaglandin E2.Biology of reproduction · 2015Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E2 (PGE2) has been reported to modulate angiogenesis, the process of new blood vessel formation, by promoting proliferation, migration and tube formation of endothelial cells. Endothelial progenitor cells are known as a subset of circulating bone marrow mononuclear cells that have the capacity to differentiate into endothelial cells. However, the mechanism underlying the stimulatory effects of PGE2 and its specific receptors on bone marrow-derived cells (BMCs) in angiogenesis has not been fully characterized. Treatment with PGE2 significantly increased the differentiation and migration of BMCs. Also, the markers of differentiation to endothelial cells, CD31 and von Willebrand factor, and the genes associated with migration, matrix metalloproteinases 2 and 9, were significantly upregulated. This upregulation was abolished by dominant-negative AMP-activated protein kinase (AMPK) and AMPK inhibitor but not protein kinase, a inhibitor. As a functional consequence of differentiation and migration, the tube formation of BMCs was reinforced. Along with altered BMCs functions, phosphorylation and activation of AMPK and endothelial nitric oxide synthase, the target of activated AMPK, were both increased which could be blocked by EP4 blocking peptide and simulated by the agonist of EP4 but not EP1, EP2 or EP3. The pro-angiogenic role of PGE2 could be repressed by EP4 blocking peptide and retarded in EP4(+/-) mice. Therefore, by promoting the differentiation and migration of BMCs, PGE2 reinforced their neovascularization by binding to the receptor of EP4 in an AMPK-dependent manner. PGE2 may have clinical value in ischemic heart disease.
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