Document Detail


Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury.
MedLine Citation:
PMID:  20434187     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Estrogen may protect against the development of cardiovascular disease. Recently, a receptor known as GPR30 that seems to mediate estrogen's nongenomic effects has been identified. We hypothesized that the activation of GPR30 protects cardiac function and decreases myocardial inflammation after global ischemia/reperfusion (I/R). METHODS: Hearts from male Sprague-Dawley rats were perfused via Langendorff and treated with either (1) vehicle; (2) 10 nm of the GPR30 agonist, G-1; or (3) 100 nm of G-1; they then were subjected to 25 minutes of ischemia and 40 minutes of reperfusion. Cardiac functional parameters were measured continuously. Ventricular tissue was analyzed for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. RESULTS: At end-reperfusion, the left ventricular developed pressure in the 100-nm G-1 group was improved compared with vehicle (26% +/- 12% equilibrium vs 54% +/- 9% equilibrium; P < .05). Similar findings were noted when comparing the 100-nm G-1 group with the vehicle in terms of +dP/dt (53% +/- 12% equilibrium vs 26% +/- 19%, respectively; P < .05) and -dP/dt (56% +/- 15% equilibrium vs 22% +/- 16% equilibrium, respectively; P < .05). TNF-alpha, IL-1beta, and IL-6 levels were lower in myocardium of the 100-nm G-1 group compared with the vehicle (P < .05). CONCLUSION: The GPR30 agonist, G-1, improves functional recovery and decreases myocardial inflammation after global I/R. GPR30 may play an important role in estrogen's ability to protect the heart against I/R injury.
Authors:
Brent R Weil; Mariuxi C Manukyan; Jeremy L Herrmann; Yue Wang; Aaron M Abarbanell; Jeffrey A Poynter; Daniel R Meldrum
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Surgery     Volume:  148     ISSN:  1532-7361     ISO Abbreviation:  Surgery     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-16     Completed Date:  2010-08-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0417347     Medline TA:  Surgery     Country:  United States    
Other Details:
Languages:  eng     Pagination:  436-43     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2010 Mosby, Inc. All rights reserved.
Affiliation:
Department of Surgery, Indiana University School of Medicine, Indianapolis, IN, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclopentanes / pharmacology
Estrogens / metabolism
Heart / drug effects,  physiopathology
Inflammation Mediators / metabolism
Interleukin-1beta / metabolism
Interleukin-6 / metabolism
Male
Myocardial Reperfusion Injury / drug therapy,  metabolism*,  physiopathology,  prevention & control*
Myocardium / metabolism*
Quinolines / pharmacology
Rats
Rats, Sprague-Dawley
Receptors, G-Protein-Coupled / agonists,  metabolism*
Signal Transduction
Tumor Necrosis Factor-alpha / metabolism
Grant Support
ID/Acronym/Agency:
F32HL092718/HL/NHLBI NIH HHS; F32HL092719/HL/NHLBI NIH HHS; F32HL093987/HL/NHLBI NIH HHS; R01GM070628/GM/NIGMS NIH HHS; R01HL085595/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone; 0/Cyclopentanes; 0/Estrogens; 0/GPR30 protein, rat; 0/Inflammation Mediators; 0/Interleukin-1beta; 0/Interleukin-6; 0/Quinolines; 0/Receptors, G-Protein-Coupled; 0/Tumor Necrosis Factor-alpha

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