ArticleCirculation2013
Cell selective cardiovascular biology of microsomal prostaglandin E synthase-1.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- Decreased PGE₂ content reduces MMP-1 activity and consequently increases collagen density in human varicose vein.PloS one · 2014Trial
- Myeloid Cell mPGES-1 Deletion Attenuates Calcium Phosphate-induced Abdominal Aortic Aneurysm in Male Mice.Inflammation · 2025Article
- Aspirin treatment for unruptured intracranial aneurysms: Focusing on its anti-inflammatory role.Heliyon · 2024Review
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Role of prostanoids, nitric oxide and endothelin pathways in pulmonary hypertension due to COPD.Frontiers in medicine · 2023Review
- Article
- Imbalanced prostanoid release mediates cigarette smoke-induced human pulmonary artery cell proliferation.Respiratory research · 2022Article
- Endothelial Tenascin-X Is Going With the Flow.Circulation research · 2022Article
- In Silico, In Vitro, and In Vivo Analysis of Tanshinone IIA and Cryptotanshinone fromBiomolecules · 2022Article
- Epithelial Cell-specific Deletion of Microsomal Prostaglandin E Synthase-1 Does Not Influence Colon Tumor Development in Mice.Journal of cancer prevention · 2021Article
- Targeted delivery of mPGES-1 inhibitors to macrophages via the folate receptor-β for inflammatory pain.Bioorganic & medicinal chemistry letters · 2021Article
- Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice.The Journal of pharmacology and experimental therapeutics · 2019Article
- Time-Dependent Hypotensive Effect of Aspirin in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
- Protective Role of mPGES-1 (Microsomal Prostaglandin E Synthase-1)-Derived PGEArteriosclerosis, thrombosis, and vascular biology · 2018Article
- Inhibition of microsomal PGE synthase-1 reduces human vascular tone by increasing PGIBritish journal of pharmacology · 2017Article
- Deficiency of mPGES-1 exacerbates renal fibrosis and inflammation in mice with unilateral ureteral obstruction.American journal of physiology. Renal physiology · 2017Article
- Cardiovascular effects of cyclooxygenase-2 inhibitors: a mechanistic and clinical perspective.British journal of clinical pharmacology · 2016Review
- Cardiovascular Consequences of Prostanoid I Receptor Deletion in Microsomal Prostaglandin E Synthase-1-Deficient Hyperlipidemic Mice.Circulation · 2016Article
- Role of COX-2-derived PGE2 on vascular stiffness and function in hypertension.British journal of pharmacology · 2016Article
- An Update of Microsomal Prostaglandin E Synthase-1 and PGE2 Receptors in Cardiovascular Health and Diseases.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGlobal deletion of microsomal prostaglandin E synthase 1 (mPGES-1) in mice attenuates the response to vascular injury without a predisposition to thrombogenesis or hypertension. However, enzyme deletion results in cell-specific differential use by prostaglandin synthases of the accumulated prostaglandin H(2) substrate. Here, we generated mice deficient in mPGES-1 in vascular smooth muscle cells, endothelial cells, and myeloid cells further to elucidate the cardiovascular function of this enzyme. METHODS AND
resultsVascular smooth muscle cell and endothelial cell mPGES-1 deletion did not alter blood pressure at baseline or in response to a high-salt diet. The propensity to evoked macrovascular and microvascular thrombogenesis was also unaltered. However, both vascular smooth muscle cell and endothelial cell mPGES-1-deficient mice exhibited a markedly exaggerated neointimal hyperplastic response to wire injury of the femoral artery in comparison to their littermate controls. The hyperplasia was associated with increased proliferating cell nuclear antigen and tenascin-C expression. In contrast, the response to injury was markedly suppressed by myeloid cell depletion of mPGES-1 with decreased hyperplasia, leukocyte infiltration, and expression of proliferating cell nuclear antigen and tenascin-C. Conditioned medium derived from mPGES-1-deficient macrophages less potently induced vascular smooth muscle cell proliferation and migration than that from wild-type macrophages.
conclusionsDeletion of mPGES-1 in the vasculature and myeloid cells differentially modulates the response to vascular injury, implicating macrophage mPGES-1 as a cardiovascular drug target.
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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.