Physiological Concentration of 17β-Estradiol on Sympathetic Reinnervation in Ovariectomized Infarcted Rats

Lee, Tsung-Ming; Lin, Mei-Shu; Chang, Nen-Chung

doi:10.1210/en.2007-0859

Cited by 10 publications

(8 citation statements)

References 52 publications

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“…These results are in agreement with several other studies that have shown estrogen levels and uterine weight decrease after ovariectomy [52][53][54]. This study also showed that sarcolemmal ERα expression was markedly increased in ventricular tissue from ovariectomized mice (6-weeks post-surgery).…”

Section: Sshrs and Hormonal Variationssupporting

confidence: 93%

Expression, Distribution and Regulation of Sex Steroid Hormone Receptors in Mouse Heart

Lizotte

Grandy

Tremblay

et al. 2009

Cell Physiol Biochem

104

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The effects of sex hormones on the heart are dependent on the presence and distribution of sex steroid hormone receptors (SSHR) in cardiac tissue. This study used subcellular fractionation, Western blot analysis and densitometry to characterize the subcellular 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 ventricular tissue ERα was primarily found in the sarcolemma, whereas ERβ and AR were predominantly located in the nucleus and cytosol. Interestingly, ERα expression was greater in the ventricles compared to the atria, whereas ERβ and AR expression were similar in both heart chambers. Furthermore, the distribution and abundance of SSHR in the atria and ventricles did not differ between sexes. This study also showed that a reduction in hormone levels (as a result of ovariectomy) resulted in a significant increase in the abundance of ERα in the ventricular sarcolemmal 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 subcellular location of SSHRs.

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Section: Sshrs and Hormonal Variationssupporting

confidence: 93%

Expression, Distribution and Regulation of Sex Steroid Hormone Receptors in Mouse Heart

Lizotte

Grandy

Tremblay

et al. 2009

Cell Physiol Biochem

104

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show abstract

“…Considering that the half-life of testosterone is much shorter than that of E 2 , and that testosterone was measured 1 day after MT injection, it is not surprising that no amount of testosterone was detected in GNX + MT female rats. The plasma E 2 level (170 pg/ml) in the control GNX ( table 3 ) appeared to be high, compared to that (about 19 pg/ml) found in another study [11] . Although the plasma E 2 level was high, the uterine weight (500 mg/kg BW) seems to be comparable to others [12] .…”

Section: Discussioncontrasting

confidence: 57%

Effects of Gender, Gonadectomy and Sex Hormones on Growth and Plasma Cholesterol Level in Rats

Lee

Kang²,

Kim³

2008

Ann Nutr Metab

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Background/Aims: No studies have clearly demonstrated how sex hormones are involved in the observed gender difference in growth and plasma cholesterol levels in animals fed hypercholesterolemic diets. This study was conducted to determine the effects of gender, gonadectomy (GNX), and sex hormones on growth, plasma cholesterol and cortisol levels in Sprague-Dawley rats. Methods: In the first of two experiments, equal numbers of male and female 4-week-old rats were divided into three groups: sham-operated control, GNX, or GNX + 17α-methyltestosterone (MT). The rats were fed a hypercholesterolemic diet for 4 weeks. In a second experiment, 24 GNX females were equally divided into three groups: control, 17β-estradiol (E₂), or MT. These rats were fed a normocholesterolemic diet for 3 weeks. Results: The average total plasma cholesterol level in female rats was twice that in male rats. MT administration to GNX male and GNX female rats decreased plasma cholesterol levels by 23 and 45%, respectively. Weekly intramuscular injection of E₂ markedly suppressed growth while increasing plasma cortisol levels in GNX female rats. Conclusion: Testosterone decreases plasma cholesterol levels in rats fed a hypercholesterolemic diet and E₂ suppresses growth of rats, inducing the secretion of hormones that increase with stress.

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“…While the present study provides strong evidence that sympathetic hyperinnervation requires increased numbers of macrophages, additional studies with larger numbers of rats and a more protracted time course will be required to assess any impact of clodronate liposome treatment on post-infarct survival. Similarly, the extent to which other factors reported to modulate infarct sympathetic hyperinnervation, which include estrogen [33], statin treatment [32], and glucocorticoids [14], affect macrophage dynamics and NGF expression remain to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

Macrophage depletion suppresses sympathetic hyperinnervation following myocardial infarction

et al. 2009

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Myocardial infarction induces sympathetic axon sprouting adjacent to the necrotic region, and this has been implicated in the etiology of arrhythmias resulting in sudden cardiac death. Previous studies show that nerve growth factor (NGF) is essential for enhanced post-infarct sympathetic sprouting, but the cell types necessary to supply this neurotrophic protein are unknown. The objective of the present study was to determine whether macrophages, which are known to synthesize NGF, are necessary for post-infarct cardiac sympathetic sprouting. Ovariectomized female rats received left coronary artery ligation or sham operation, followed by intravenous injection of liposomes containing saline vehicle or clodronate, which kills macrophages. Sham-operated myocardium contained some sympathetic axons, few myofibroblasts and T cells and no CD-68-positive macrophages. In rats receiving saline liposomes through 7 days post-ligation, the posterolateral infarct border contained numerous myofibroblasts, macrophages and T cells, and sympathetic innervation was increased twofold. Treatment with clodronate liposomes reduced macrophage numbers by 69%, while myofibroblast area was reduced by 23% and T cell number was unaffected. Clodronate liposome treatment reduced sympathetic axon density to levels comparable to the uninfarcted heart. NGF protein content measured in western blots was reduced to 33% of that present in infarcts where rats received saline-containing liposomes. Tissue morphometry confirmed that NGF immunostaining was dramatically reduced, and this was attributable primarily to reduced macrophage content. These results show that macrophage destruction markedly reduces post-infarction levels of NGF and that the presence of elevated numbers of macrophages is obligatory for development of sympathetic hyperinnervation following myocardial infarction.

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Physiological Concentration of 17β-Estradiol on Sympathetic Reinnervation in Ovariectomized Infarcted Rats

Cited by 10 publications

References 52 publications

Expression, Distribution and Regulation of Sex Steroid Hormone Receptors in Mouse Heart

Expression, Distribution and Regulation of Sex Steroid Hormone Receptors in Mouse Heart

Effects of Gender, Gonadectomy and Sex Hormones on Growth and Plasma Cholesterol Level in Rats

Macrophage depletion suppresses sympathetic hyperinnervation following myocardial infarction

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