Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability

Terrell, Andrew M.; Crisostomo, Paul R.; Markel, Troy A.; Wang, Meijing; Abarbanell, Aaron M.; Herrmann, Jeremy L.; Meldrum, Daniel R.

doi:10.1016/j.jss.2007.05.021

Cited by 19 publications

(9 citation statements)

References 38 publications

(35 reference statements)

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“…Since LVEDP elevations are considered indexes of cardiac dysfunction, as observed in ischemia/ reperfusion [27], we speculate that the cardiodepression elicited by 17βE2 is not detrimental for the heart. This agrees with the cardioprotection elicited by nanomolar estrogen doses in male rats subject to ischemia/ reperfusion [28]. Also in women it has been reported by clinical studies that endogenous estrogens (as in premenopausal period) contribute to reduce the risk for cardiovascular events [29].…”

Section: Discussionsupporting

confidence: 88%

Crucial Role of Phospholamban Phosphorylation and S-Nitrosylation in the Negative Lusitropism Induced by 17β-estradiol in the Male Rat Heart

Filice

Angelone²,

Francesco³

et al. 2011

Cell Physiol Biochem

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Background/Aims: 17β-estradiol (17βE2) plays an important cardiovascular role by activating estrogen receptors (ER) α and ERβ. Previous studies demonstrated that the novel estrogen G protein-coupled receptor (GPR30/GPER) mediates estrogen action in different tissues. We have recently shown in the rat heart that 17βE2 elicits negative inotropism through ERα, ERβ and GPR30, by triggering activation of ERK1/2, phosphatidylinositol 3-kinase (PI3K), protein kinase A (PKA) and endothelial Nitric Oxide synthase (eNOS) signaling. Methods: In the present study, using the isolated and Langendorff-perfused rat heart as a model system we analyzed: i) whether and to which extent 17βE2 modifies mammalian ventricular myocardial relaxation (lusitropism); ii) the type of ERs and the signaling pathways involved in this effect. Results: We found that 17βE2 negatively modulated the ventricular lusitropic performance. This effect, which partially involved the vascular endothelium, recruited ERβ and occurred via PI3K, eNOS-NO-cGMP-protein kinase G (PKG) transduction cascade. Of note, 17βE2-mediated negative lusitropism associated with a modification of phospholamban (PLN) phosphorylation and S-nitrosylation (SNO) both in isolated Langendorff rat heart and in isolated cardiomyocytes. Conclusion: Taken together, our results allow including 17βE2 to the family of substances that control ventricular relaxation. This is of relevance in relation not only to the normal endocrine control of cardiac function, but also to physio-pathologic conditions characterized by an altered ventricular diastolic performance.

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Section: Discussionsupporting

confidence: 88%

Crucial Role of Phospholamban Phosphorylation and S-Nitrosylation in the Negative Lusitropism Induced by 17β-estradiol in the Male Rat Heart

Filice

Angelone²,

Francesco³

et al. 2011

Cell Physiol Biochem

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“…Despite the protection afforded by administering the ER modulators before ischemia (preconditioning effect), a post-ischemic treatment approach (post-conditioning effect) with these ER-regulated pharmacological agents might be more clinically relevant. Recently, acute post-ischemic infusion with E2 has been found to improve left ventricular myocardial function after 25 min of ischemia (Terrell et al 2008). To further distinguish which ER activation mediates this post-conditioning effect, the post-ischemic infusion was replaced with PPT or DPN.…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Estrogen Receptor Activation and Cardioprotection in Ischemia Reperfusion Injury

Deschamps

Murphy

Sun

2010

Trends in Cardiovascular Medicine

131

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Pre-menopausal females have a comparably lower incidence of cardiovascular disease than their male counterparts. Although estrogen and activation of estrogen receptors (ER) have been found to contribute to female protection, the complex mechanisms involved are unclear. Besides altering gene transcription, estrogen could elicit its cardioprotective effect via ER-mediated nongenomic signaling pathways. In addition to the two classic nuclear ER isoforms, ERα and ERβ, a G-protein coupled ER (GPR30 or GPER), has been found to be expressed in cardiomyocytes and plays an acute cardioprotective role in ischemia reperfusion (I/R) injury. By using isoform-specific ER knockout mouse models and/or their specific modulators, the mechanisms of the different ERs involved in cardioprotection have been explored. In this review, we will focus on the signaling pathways leading to cardioprotection in I/R injury after ER activation and discuss the possibility and promise of specific ER modulators to treat ischemic heart diseases.

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“…Administration of E2 attenuates cardiac dysfunction, suggesting that E2 may be involved in mediating this cardioprotection in females 4. Additionally, post-injury treatment with E2, demonstrates protection of myocardial function against I/R and may have clinical potential in the treatment of acute myocardial infarction 6. In this study, we further determined by what mechanisms E2 conveys this acute cardiac protection following I/R.…”

Section: Discussionmentioning

confidence: 88%

“…However, with respect to therapeutic potential in the treatment of acute myocardial infarction, post-insult administration of estrogen has more clinical appeal. Recently, our group demonstrated that post-ischemic infusion of 17β-estradiol (E2) throughout the 40 minute reperfusion period improved left ventricular (LV) function compared to control 6.…”

Section: Introductionmentioning

confidence: 99%

Acute postischemic treatment with estrogen receptor-α agonist or estrogen receptor-β agonist improves myocardial recovery

Vornehm

Wang

Abarbanell

et al. 2009

Surgery

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Background-Female hearts following ischemia/reperfusion (I/R) injury demonstrate improved functional recovery compared to male, which suggests a protective role for estrogen. Acute postischemic treatment with 17-β-estradiol (E2) attenuates myocardial dysfunction. However, it is unknown by which estrogen receptor (ER) E2 mediates this acute cardioprotection during I/R. Therefore, we hypothesize that post-ischemic infusion of the selective ER-α agonist (PPT) or the selective ER-β agonist (DPN) will improve myocardial function following I/R.

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Postischemic Infusion of 17-β-Estradiol Protects Myocardial Function and Viability

Cited by 19 publications

References 38 publications

Crucial Role of Phospholamban Phosphorylation and S-Nitrosylation in the Negative Lusitropism Induced by 17β-estradiol in the Male Rat Heart

Crucial Role of Phospholamban Phosphorylation and S-Nitrosylation in the Negative Lusitropism Induced by 17β-estradiol in the Male Rat Heart

Estrogen Receptor Activation and Cardioprotection in Ischemia Reperfusion Injury

Acute postischemic treatment with estrogen receptor-α agonist or estrogen receptor-β agonist improves myocardial recovery

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