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Oestrogen modulates cardiac ischaemic remodelling through oestrogen receptor‐specific mechanisms
Author(s) -
Babiker F. A.,
Lips D. J.,
Delvaux E.,
Zandberg P.,
Janssen B. J. A.,
Prinzen F.,
Van Eys G.,
Grohé C.,
Doevendans P. A.
Publication year - 2007
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2006.01633.x
Subject(s) - medicine , placebo , endocrinology , ovariectomized rat , myocardial infarction , receptor , estrogen receptor , coronary artery disease , sham surgery , ligation , estrogen , cardiology , pathology , breast cancer , alternative medicine , cancer
Aim: Observational and clinical studies suggest different responses upon sex hormone replacement therapy in ischaemic heart disease. Few studies, however, have examined the impact of oestrogen receptor‐dependent mechanisms on the extent of injury after myocardial infarction (MI). Therefore, we set out to evaluate the effect of oestrogen (E2) replacement on infarct size and remodelling, and the respective role of the oestrogen receptors (ER) α and ‐ β in this process, using ER α ‐ and ER β ‐deficient mice. Methods: Wild type (WT) (ER α +/+ and ER β +/+ ), ER α ‐deficient (ER α −/− ) and ER β ‐deficient (ER β −/− ) mice were ovariectomized and subsequently supplemented with E2 or placebo using subcutaneous 60‐day release pellets. MI was induced by left coronary artery ligation. Two weeks following MI, haemodynamic function was assessed and infarct size was determined. Results: There was no significant difference in infarct size between E2‐ or placebo‐treated WT (ER α +/+ and ER β +/+ ) mice. Surprisingly, E2 treatment did result in smaller infarct sizes in ER α −/− mice, but increased the infarct size in ER β −/− mice. Increase of the left ventricular mass post‐MI was significantly larger in the E2‐treated ER α −/− animals compared with placebo‐treated animals. E2 treatment also significantly increased post‐MI mortality in ER α +/+ , ER β +/+ and ER α −/− animals, but not in ER β −/− mice. Conclusions: Although E2 modulates the infarct size in ER α −/− , it also appears to be responsible for the higher mortality following MI. ER β appears to be the receptor involved in the modulating effects of E2 in the infarcted heart.