ArticleProceedings of the National Academy of Sciences of the United States of America2014
Myeloid cell microsomal prostaglandin E synthase-1 fosters atherogenesis in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Experimental Research Progress of mPGES-1 Inhibitor 2,5- dimethylcelecoxib in Various Diseases.Current medicinal chemistry · 2026Review
- Myeloid Cell mPGES-1 Deletion Attenuates Calcium Phosphate-induced Abdominal Aortic Aneurysm in Male Mice.Inflammation · 2025Article
- Disruption of the PGEbioRxiv : the preprint server for biology · 2024Article
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Circadian control of ConA-induced acute liver injury and inflammatory response via Bmal1 regulation of Junb.JHEP reports : innovation in hepatology · 2023Article
- LDL-Dependent Regulation of TNFα/PGEInflammation · 2023Article
- The Link between Prostanoids and Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022Review
- 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
- Understanding the Exchange of Systemic HDL Particles Into the Brain and Vascular Cells Has Diagnostic and Therapeutic Implications for Neurodegenerative Diseases.Frontiers in physiology · 2021Review
- Targeting microsomal prostaglandin E synthase 1 to develop drugs treating the inflammatory diseases.American journal of translational research · 2021Article
- Bmal1 Deletion in Myeloid Cells Attenuates Atherosclerotic Lesion Development and Restrains Abdominal Aortic Aneurysm Formation in Hyperlipidemic Mice.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Sodium Orthovanadate Changes Fatty Acid Composition and Increased Expression of Stearoyl-Coenzyme A Desaturase in THP-1 Macrophages.Biological trace element research · 2020Article
- Myeloid Cell mPges-1 Deletion Attenuates Mortality Without Affecting Remodeling After Acute Myocardial Infarction in Mice.The Journal of pharmacology and experimental therapeutics · 2019Article
- Lipopolysaccharide (LPS)-mediated priming of toll-like receptor 4 enhances oxidant-induced prostaglandin EInternational immunopharmacology · 2018Article
- Lipoproteins and lipoprotein mimetics for imaging and drug delivery.Advanced drug delivery reviews · 2016Review
- Role of COX-2-derived PGE2 on vascular stiffness and function in hypertension.British journal of pharmacology · 2016Article
- PGE2, Kidney Disease, and Cardiovascular Risk: Beyond Hypertension and Diabetes.Journal of the American Society of Nephrology : JASN · 2016Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vascular cells differentially regulates the response to vascular injury, reflecting distinct effects of mPGES-1-derived PGE2 in these cell types on discrete cellular components of the vasculature. The cell selective roles of mPGES-1 in atherogenesis are unknown. Mice lacking mPGES-1 conditionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1-KOs), or endothelial cells (EC-mPGES-1-KOs) were crossed into hyperlipidemic low-density lipoprotein receptor-deficient animals. En face aortic lesion analysis revealed markedly reduced atherogenesis in Mac-mPGES-1-KOs, which was concomitant with a reduction in oxidative stress, reflective of reduced macrophage infiltration, less lesional expression of inducible nitric oxide synthase (iNOS), and lower aortic expression of NADPH oxidases and proinflammatory cytokines. Reduced oxidative stress was reflected systemically by a decline in urinary 8,12-iso-iPF2α-VI. In contrast to exaggeration of the response to vascular injury, deletion of mPGES-1 in VSMCs, ECs, or both had no detectable phenotypic impact on atherogenesis. Macrophage foam cell formation and cholesterol efflux, together with plasma cholesterol and triglycerides, were unchanged as a function of genotype. In conclusion, myeloid cell mPGES-1 promotes atherogenesis in hyperlipidemic mice, coincident with iNOS-mediated oxidative stress. By contrast, mPGES-1 in vascular cells does not detectably influence atherogenesis in mice. This strengthens the therapeutic rationale for targeting macrophage mPGES-1 in inflammatory cardiovascular diseases.
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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.