A sexually dimorphic distribution pattern of the novel estrogen receptor G-protein-coupled receptor 30 in some brain areas of the hamster

Canonaco, Marcello; Giusi, Giuseppina; Madeo, Antonio; Facciolo, Rosa Maria; Lappano, Rosamaria; Canonaco, Alessia; Maggiolini, Marcello

doi:10.1677/joe-07-0392

Cited by 45 publications

(24 citation statements)

References 26 publications

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“…Moreover, a high level of GPER immunoreactivity was observed in the striatum and thalamus in both sexes. These findings are, however, in contrast to those of Canonaco et al [22] who reported that a sexually dimorphic GPER expression pattern occurs in the hypothalamus and thalamus of the hamster. Nevertheless, there is accumulating evidence that GPER distribution in the brain is typically quite similar between males and females.…”

Section: Discussioncontrasting

confidence: 99%

Stroke Increases G Protein-Coupled Estrogen Receptor Expression in the Brain of Male but Not Female Mice

et al. 2013

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The novel estrogen receptor, G protein-coupled estrogen receptor (GPER, previously named GPR30), is widely distributed throughout the male and female brain and, thus, could potentially play a role in estrogen-mediated neuroprotective effects in diseases such as stroke. We hypothesized that GPER distribution and expression in the brain of male, intact female, and ovariectomized (OVX) mice is increased after 0.5 h middle cerebral artery occlusion. Using immunohistochemistry, we found that ischemia reperfusion increased GPER distribution in the peri-infarct brain regions of male mice, but surprisingly not in intact females or OVX mice. Similar differences were observed in the male and female human brain after stroke. In contrast, GPER distribution was decreased in the infarct core of all mice examined. Furthermore, GPER immunofluorescence was co-localized with the endothelial cell marker, von Willebrand factor, and the neuronal marker, NeuN. Consistent with the immunohistochemical findings, Western blot analysis showed GPER expression is only elevated in the ischemic hemisphere of male mice. Moreover, GPER mRNA expression in males was elevated at 4 h but had returned to baseline by 24 h. In conclusion, these findings indicate that GPER may be a potential therapeutic target after stroke, especially in males, in whom estrogen therapy is not feasible.

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Section: Discussioncontrasting

confidence: 99%

Stroke Increases G Protein-Coupled Estrogen Receptor Expression in the Brain of Male but Not Female Mice

et al. 2013

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“…3A). In addition, G-1-induced relaxation was unaffected by pretreating arteries with 10 M 1 H- [1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a selective inhibitor of guanylyl cyclase activity (n ϭ 5; data not shown). However, similar to 17␤-estradiol, the relaxation effect of G-1 was dependent upon potassium efflux from CASM cells.…”

Section: Resultsmentioning

confidence: 95%

Activation of G protein-coupled estrogen receptor induces endothelium-independent relaxation of coronary artery smooth muscle

Barman

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

100

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Estrogens can either relax or contract arteries via rapid, nongenomic mechanisms involving classic estrogen receptors (ER). In addition to ERα and ERβ, estrogen may also stimulate G protein-coupled estrogen receptor 1 (GPER) in nonvascular tissue; however, a potential role for GPER in coronary arteries is unclear. The purpose of this study was to determine how GPER activity influenced coronary artery reactivity. In vitro isometric force recordings were performed on endothelium-denuded porcine arteries. These studies were augmented by RT-PCR and single-cell patch-clamp experiments. RT-PCR and immunoblot studies confirmed expression of GPER mRNA and protein, respectively, in smooth muscle from either porcine or human coronary arteries. G-1, a selective GPER agonist, produced a concentration-dependent relaxation of endothelium-denuded porcine coronary arteries in vitro. This response was attenuated by G15, a GPER-selective antagonist, or by inhibiting large-conductance calcium-activated potassium (BK(Ca)) channels with iberiotoxin, but not by inhibiting NO signaling. Last, single-channel patch-clamp studies demonstrated that G-1 stimulates BK(Ca) channel activity in intact smooth muscle cells from either porcine or human coronary arteries but had no effect on channels isolated in excised membrane patches. In summary, GPER activation relaxes coronary artery smooth muscle by increasing potassium efflux via BK(Ca) channels and requires an intact cellular signaling mechanism. This novel action of estrogen-like compounds may help clarify some of the controversy surrounding the vascular effects of estrogens.

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“…Several studies have implicated hypothalamic Erk 1/2 in the regulation of energy homeostasis [46,47] and activation of the Erk 1/2 signaling pathway in the CNS mediates the anorectic effects of leptin [48] and CCK [23]. Canonaco et al, reported overlapping distribution of Erk 1/2 with GPER in most brain areas [49] of the hamster. Here, we demonstrate for the first time that female OVX GPER KO mice have reduced 17β-estradiol-induced pErk 1/2 when compared to WT mice.…”

Section: Discussionmentioning

confidence: 99%

Sexually dimorphic role of G protein-coupled estrogen receptor (GPER) in modulating energy homeostasis

Davis

Carstens

Irani

et al. 2014

Hormones and Behavior

110

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The classical estrogen receptors, estrogen receptor-α and estrogen receptor-β are well established in the regulation of body weight and energy homeostasis in both male and female mice, whereas, the role for G protein-coupled estrogen receptor 1 (GPER) as a modulator of energy homeostasis remains controversial. This study sought to determine whether gene deletion of GPER (GPER KO) alters body weight, body adiposity, food intake, and energy homeostasis in both males and females. Male mice lacking GPER developed moderate obesity and larger adipocyte size beginning at 8 weeks of age, with significant reductions in energy expenditure, but not food intake or adipocyte number. Female GPER KO mice developed increased body weight relative to WT females a full 6 weeks later than the male GPER KO mice. Female GPER KO mice also had reductions in energy expenditure, but not significant increases in body fat content. Consistent with their decrease in energy expenditure, GPER KO males and females showed significant reductions in two brown fat thermogenic proteins. GPER KO females, prior to their divergence in body weight, were less sensitive than WT females to the feeding-inhibitory effects of leptin and CCK. Additionally, body weight was not as modulated by ovariectomy or estradiol replacement in GPER KO mice. Estradiol treatment activated phosphorylated extracellular signal-regulated kinase (pERK) in WT but not GPER KO females. For the first time, GPER expression was found in the adipocyte but not the stromal fraction of adipose tissue. Together, these results provide new information elucidating a sexual dimorphism in GPER function in the development of postpubertal energy balance.

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A sexually dimorphic distribution pattern of the novel estrogen receptor G-protein-coupled receptor 30 in some brain areas of the hamster

Cited by 45 publications

References 26 publications

Stroke Increases G Protein-Coupled Estrogen Receptor Expression in the Brain of Male but Not Female Mice

Stroke Increases G Protein-Coupled Estrogen Receptor Expression in the Brain of Male but Not Female Mice

Activation of G protein-coupled estrogen receptor induces endothelium-independent relaxation of coronary artery smooth muscle

Sexually dimorphic role of G protein-coupled estrogen receptor (GPER) in modulating energy homeostasis

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