A novel estrogen receptor gper inhibits mitochondria permeability transition pore opening and protects the heart against ischemia-reperfusion injury
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Several studies have recently demonstrated that G protein-coupled receptor 30 (GPER) can directly bind to estrogen and mediate its action. We investigated the role and the mechanism of estrogen-induced cardioprotection after ischemia-reperfusion using a specific GPER agonist G1. Isolated hearts from male mice were perfused using Langendorff technique with oxygenated (95% O(2) and 5% CO(2)) Krebs Henseleit buffer (control), with G1 (1 microM), and G1 (1 microM) together with extracellular signal-regulated kinase (Erk) inhibitor PD-98059 (5 microM). After 20 min of perfusion, hearts were subjected to 20 min global normothermic (37 degrees C) ischemia followed by 40 min reperfusion. Cardiac function was measured, and myocardial necrosis was evaluated by triphenyltetrazolium chloride staining at the end of the reperfusion. Mitochondria were isolated after 10 min of reperfusion to assess the Ca(2+) load required to induce mitochondria permeability transition pore (mPTP) opening. G1-treated hearts developed better functional recovery with higher rate pressure product (RPP, 6140 +/- 264 vs. 2,640 +/- 334 beats mmHg(-1) min(-1), P < 0.05). The infarct size decreased significantly in G1-treated hearts (21 +/- 2 vs. 46 +/- 3%, P < 0.001), and the Ca(2+) load required to induce mPTP opening increased (2.4 +/- 0.06 vs. 1.6 +/- 0.11 microM/mg mitochondrial protein, P < 0.05) compared with the controls. The protective effect of G1 was abolished in the presence of PD-98059 [RPP: 4,120 +/- 46 beats mmHg(-1) min(-1), infarct size: 53 +/- 2%, and Ca(2+) retention capacity: 1.4 +/- 0.11 microM/mg mitochondrial protein (P < 0.05)]. These results suggest that GPER activation provides a cardioprotective effect after ischemia-reperfusion by inhibiting the mPTP opening, and this effect is mediated by the Erk pathway.
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Activation of GPER is associated with the inhibition of mPTP opening, an effect mediated by the ERK pathway.
“Activation of GPER is associated with the inhibition of mPTP opening, an effect mediated by the ERK pathway (125).”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [125]
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MitoBKCa channel is functionally associated with its regulatory β1 subunit in cardiac mitochondria
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- Authors
- Bopassa, J. C., Eghbali, M., Toro, L., & Stefani, E.
- Affiliations
- Division of Molecular Medicine, Department of Anesthesiology,
- University of California, Los Angeles (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2010-01
- Volume
- 298
- Issue
- 1
- Pages
- H16-H23
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- PMC
- PMC2806134
- OpenAlex
- W2151524159
- Cited by
- 197
- References
- 39
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 11 · 2023: 11 · 2022: 15 · 2021: 15 · 2020: 15 · 2019: 19 · 2018: 14 · 2017: 12 · 2016: 13 · 2015: 13 · 2014: 11 · 2013: 10 · 2012: 13
- FWCI
- 7.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL 54970, P01HL080111, R01HL089876, R01HL088640, HL-088640, HL080111, R01HL054970, HL-089876)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- G protein-coupled receptor 30, estrogen receptor, G1 agonist, cardioprotection, myocardial ischemia-reperfusion injury, ERK signaling, PD98059, calcium retention capacity, infarct size, rate-pressure product, estrogen cardioprotection
- MeSH terms
- Adenosine Triphosphate, Animals, Enzyme Inhibitors, Flavonoids, Heart Diseases, Hemodynamics, Male, Mice, Inbred C57BL, Mitochondria, Heart, Myocardial Infarction, Myocardium, Permeability, Blotting, Western, Reperfusion Injury, Oxidative Stress, Protective Agents, Reverse Transcriptase Polymerase Chain Reaction, Extracellular Signal-Regulated MAP Kinases, Mice, In Vitro Techniques
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