75
Original Paper
Cell Physiol Biochem 2009;23:75-86
Accepted: November 20, 2008
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Expression, Distribution and Regulation of Sex
Steroid Hormone Receptors in Mouse Heart
Eric Lizotte
1,2
, Scott A. Grandy
1,2
, Annie Tremblay
1,2
, Bruce G. Allen
1,3
and Céline Fiset
1,2
1
Research Center, Montreal Heart Institute,
2
Faculty of Pharmacy, Université de Montréal,
3
Department of
Medicine, Université de Montréal, Montréal, Quebec
Dr. Céline Fiset
Research Center, Montreal Heart Institute
5000 Belanger Street, Montreal, Quebec, H1T 1C8 (Canada)
Tel. +1 514-376-3330 (Ext. 3025); Fax +1 514-376-1355
E-Mail celine.fiset@umontreal.ca
Key Words
Cardiac Ovariectomy Subcellular distribution Pro-
tein fraction
Abstract
The effects of sex hormones on the heart are de-
pendent on the presence and distribution of sex ster-
oid hormone receptors (SSHR) in cardiac tissue. This
study used subcellular fractionation, Western blot
analysis and densitometry to characterize the sub-
cellular distribution and abundance of estrogen
receptor (ER) α, ERβ and androgen receptor (AR) in
atrial and ventricular tissue from male and female
mice. The results showed that in both atrial and ven-
tricular tissue ERα was primarily found in the sarco-
lemma, whereas ERβ and AR were predominantly lo-
cated in the nucleus and cytosol. Interestingly, ERα
expression was greater in the ventricles compared to
the atria, whereas ERβ and AR expression were simi-
lar in both heart chambers. Furthermore, the distri-
bution and abundance of SSHR in the atria and ven-
tricles did not differ between sexes. This study also
showed that a reduction in hormone levels (as a re-
sult of ovariectomy) resulted in a significant increase
in the abundance of ERα in the ventricular sarco-
lemmal fraction. Overall, the results suggest ERα,
ERβ and AR distribution and expression are not sex
dependent in the mouse heart. However, it appears
that ERα expression is chamber specific and that, in
certain cases, hormone levels can modulate the sub-
cellular location of SSHRs.
Introduction
Cardiovascular diseases are the leading cause of
mortality for both men and women throughout most of
the industrialized world [1-7]. Interestingly, women tend
to develop heart disease later in life than men [8, 9]. In
fact, the incidence of cardiovascular diseases only begins
to steadily increase in women after the onset of
menopause [10]. It is believed that the late onset of
cardiovascular disease in women is partially attributable
to sex differences in sex steroid hormones [8].
Specifically, endogenous estrogen may have a
cardioprotective effect in premenopausal women [9].
Furthermore, evidence suggests that the male sex
hormones may play a role in the development of certain
types of cardiovascular disease [11, 12]. Thus it appears