{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:38:36Z","timestamp":1791923916394,"version":"4.3.4"},"reference-count":67,"publisher":"The Endocrine Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Aldosterone (Aldo) activates both genomic and nongenomic signaling pathways in the cardiovascular system. Activation of genomic signaling pathways contributes to the adverse cardiac actions of Aldo during reperfusion injury; however, the extent nongenomic signaling pathways contribute has been difficult to identify due to lack of a specific ligand that activates only nongenomic signaling pathways. Using a pegylated aldosterone analog, aldosterone-3-carboxymethoxylamine-TFP ester conjugated to methoxypegylated amine (Aldo-PEG), we are able for the first time to distinguish between nongenomic and genomic cardiac actions of Aldo. We confirm Aldo-PEG activates phosphorylation of ERK1\/2 in rat cardiomyocyte H9c2 cells similar to Aldo and G protein-coupled receptor 30 (GPR30 or GPER) agonist G1. GPER antagonist, G36, but not mineralocorticoid receptor (MR) antagonist spironolactone, prevented ERK1\/2 phosphorylation by Aldo, Aldo-PEG, and G1. The selective nongenomic actions of Aldo-PEG are confirmed, with Aldo-PEG increasing superoxide production in H9c2 cells to similar levels as Aldo but having no effect on subcellular localization of MR. Striatin serves as a scaffold for GPER and MR, with GPER antagonist G36, but not spironolactone, restoring MR-striatin complexes. Aldo-PEG had no effect on MR-dependent transcriptional activation, whereas Aldo increased transcript levels of serum-regulated kinase 1 and plasminogen activator inhibitor-1. Using our ex vivo experimental rat model of myocardial infarction, we found aggravated infarct size and apoptosis by Aldo but not Aldo-PEG. Our studies confirm that in the heart, activation of nongenomic signaling pathways alone are not sufficient to trigger the deleterious effects of aldosterone during myocardial reperfusion injury.<\/jats:p>","DOI":"10.1210\/me.2014-1410","type":"journal-article","created":{"date-parts":[[2015,6,29]],"date-time":"2015-06-29T13:16:16Z","timestamp":1435583776000},"page":"1144-1155","source":"Crossref","is-referenced-by-count":63,"title":["Role of Nongenomic Signaling Pathways Activated by Aldosterone During Cardiac Reperfusion Injury"],"prefix":"10.1210","volume":"29","author":[{"given":"Anthony W.","family":"Ashton","sequence":"first","affiliation":[{"name":"Division of Perinatal Research (A.W.A.), Royal North Shore Hospital and The University of Sydney, Sydney 2065, Australia"},{"name":"Royal North Shore Hospital and Kolling Institute (A.W.A., T.Y.L.L., M.-C.M.-K., A.H., A.S.M.), Royal North Shore Hospital and The University of Sydney, Sydney 2065, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thi Y. L.","family":"Le","sequence":"additional","affiliation":[{"name":"Cardiovascular and Hormonal Research Laboratory, Department of Cardiology (T.Y.L.L., A.S.M.), Royal North Shore Hospital and The University of Sydney, Sydney 2065, Australia"},{"name":"Royal North Shore Hospital and Kolling Institute (A.W.A., T.Y.L.L., M.-C.M.-K., A.H., A.S.M.), Royal North Shore Hospital and The University of Sydney, Sydney 2065, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Celso E.","family":"Gomez-Sanchez","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, G. V. 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