ArticleHypertension (Dallas, Tex. : 1979)2010
The impact of microsomal prostaglandin e synthase 1 on blood pressure is determined by genetic background.
Article in Hypertension (Dallas, Tex. : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- Prostanoids in Cardiac and Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Cell-Specific Actions of the Prostaglandin E-Prostanoid Receptor 4 Attenuating Hypertension: A Dominant Role for Kidney Epithelial Cells Compared With Macrophages.Journal of the American Heart Association · 2022Article
- EP3 Receptor Deficiency Improves Vascular Remodeling and Cognitive Impairment in Cerebral Small Vessel Disease.Aging and disease · 2022Article
- Targeting microsomal prostaglandin E synthase 1 to develop drugs treating the inflammatory diseases.American journal of translational research · 2021Article
- Complex Role for E-Prostanoid 4 Receptors in Hypertension.Journal of the American Heart Association · 2019Article
- Article
- 2,5-Dimethylcelecoxib prevents pressure-induced left ventricular remodeling through GSK-3 activation.Hypertension research : official journal of the Japanese Society of Hypertension · 2017Article
- Epigenetic control of microsomal prostaglandin E synthase-1 by HDAC-mediated recruitment of p300.Journal of lipid research · 2017Article
- Deficiency of mPGES-1 exacerbates renal fibrosis and inflammation in mice with unilateral ureteral obstruction.American journal of physiology. Renal physiology · 2017Article
- Cardiovascular Consequences of Prostanoid I Receptor Deletion in Microsomal Prostaglandin E Synthase-1-Deficient Hyperlipidemic Mice.Circulation · 2016Article
- An Update of Microsomal Prostaglandin E Synthase-1 and PGE2 Receptors in Cardiovascular Health and Diseases.Oxidative medicine and cellular longevity · 2016Review
- Renal medullary (pro)renin receptor contributes to angiotensin II-induced hypertension in rats via activation of the local renin-angiotensin system.BMC medicine · 2015Article
- Skin tight: macrophage-specific COX-2 induction links salt handling in kidney and skin.The Journal of clinical investigation · 2015Article
- HuR mediates the synergistic effects of angiotensin II and IL-1β on vascular COX-2 expression and cell migration.British journal of pharmacology · 2015Article
- Role of COX-2/mPGES-1/prostaglandin E2 cascade in kidney injury.Mediators of inflammation · 2015Review
- Myeloid cell microsomal prostaglandin E synthase-1 fosters atherogenesis in mice.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Renal β-intercalated cells maintain body fluid and electrolyte balance.The Journal of clinical investigation · 2013Article
- Effect of sphingosine kinase 1 inhibition on blood pressure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Article
- Distinct roles of central and peripheral prostaglandin E2 and EP subtypes in blood pressure regulation.American journal of hypertension · 2012Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Prostaglandin (PG)E(2) has multiple actions that may affect blood pressure. It is synthesized from arachidonic acid by the sequential actions of phospholipases, cyclooxygenases, and PGE synthases. Although microsomal PGE synthase (mPGES)1 is the only genetically verified PGE synthase, results of previous studies examining the consequences of mPGES1 deficiency on blood pressure (BP) are conflicting. To determine whether genetic background modifies the impact of mPGES1 on BP, we generated mPGES1(-/-) mice on 2 distinct inbred backgrounds, DBA/1lacJ and 129/SvEv. On the DBA/1 background, baseline BP was similar between wild-type (WT) and mPGES1(-/-) mice. By contrast, on the 129 background, baseline BPs were significantly higher in mPGES1(-/-) animals than WT controls. During angiotensin II infusion, the DBA/1 mPGES1(-/-) and WT mice developed mild hypertension of similar magnitude, whereas 129-mPGES1(-/-) mice developed more severe hypertension than WT controls. DBA/1 animals developed only minimal albuminuria in response to angiotensin II infusion. By contrast, WT 129 mice had significantly higher levels of albumin excretion than WT DBA/1 and the extent of albuminuria was further augmented in 129 mPGES1(-/-) animals. In WT mice of both strains, the increase in urinary excretion of PGE(2) with angiotensin II was attenuated in mPGES1(-/-) animals. Urinary excretion of thromboxane was unaffected by angiotensin II in the DBA/1 lines but increased more than 4-fold in 129 mPGES1(-/-) mice. These data indicate that genetic background significantly modifies the BP response to mPGES1 deficiency. Exaggerated production of thromboxane may contribute to the robust hypertension and albuminuria in 129 mPGES1-deficient mice.
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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.