scholarly journals Anthocyanins Activate Membrane Estrogen Receptors With Nanomolar Potencies to Elicit a Nongenomic Vascular Response Via NO Production

2021 ◽  
Author(s):  
Camila Calfío ◽  
Francisca Donoso ◽  
J. Pablo Huidobro‐Toro
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Rapid Onset ◽  
No Production ◽  
Vascular Response ◽  
Selective Antagonists ◽  
Joint Application ◽  
Before And After ◽  
Estrogen Receptor Activity

Background The vascular pharmacodynamics of anthocyanins is only partially understood. To examine whether the anthocyanin‐induced vasorelaxation is related to membrane estrogen receptor activity, the role of ERα or GPER antagonism was ascertained on anthocyanins or 17‐β estradiol‐(E2) induced vasodilatations and NO production. Methods and Results The rat arterial mesenteric bed was perfused with either anthocyanins or corresponding 3‐O‐glycosides, or E2, to examine rapid concentration‐dependent vasorelaxations. The luminally accessible fraction of NO in mesenteric perfusates before and after anthocyanins or E2 administration was quantified. Likewise, NO‐DAF signal detected NO production in primary endothelial cells cultures incubated with anthocyanins or E2 in the absence and presence of ERα (ICI 182,780) or GPER (G‐36) selective antagonists. Anthocyanins or corresponding glycosides elicited, within minutes, vasodilation with nanomolar potencies; half maximal anthocyanin response reached 50% to 60% efficacy, in contrast to acetylcholine. The vasorelaxation is of rapid onset and exclusively endothelium‐dependent; NOS inhibition annulled the vasorelaxation. The delphinidin vascular response was not modified by 100 nmol/L atropine but significantly attenuated by joint application of ICI plus G‐36 (52±4.6 versus 8.5±1.5%), revealing the role of membrane estrogen receptors. Moreover, the anthocyanin or E2‐induced NO production was antagonized up to 70% by these antagonists. NO‐DAF signal elicited by anthocyanins was annulled by NOS inhibition or by ICI plus G‐36 addition. Conclusions The biomedical effect of anthocyanins or 3‐O‐glycosylates derivatives contained in naturally purple‐colored foods or berries is due to increased NO production, and not to the phytochemical's antioxidant potential, highlighting the nutraceutical role of natural products in cardiovascular diseases.

scholarly journals 0329 : Role of the estrogen receptor alpha (ERalpha) in the vascular response to shear stress in mice

2015 ◽  
Vol 7 (2) ◽  
pp. 142
Author(s):  
Julie Favre ◽  
Emilie Vessière ◽  
Anne-Laure Guihot ◽  
Linda Grimaud ◽  
Jean-François Arnal ◽  
...  
Keyword(s):  
Shear Stress ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Vascular Response ◽  
Receptor Alpha

scholarly journals Molecular mechanisms of estrogen receptor β-induced apoptosis and autophagy in tumors: implication for treating osteosarcoma

2019 ◽  
Vol 47 (10) ◽  
pp. 4644-4655
Author(s):  
Zheng-ming Yang ◽  
Min-fei Yang ◽  
Wei Yu ◽  
Hui-min Tao
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Critical Role ◽  
Osteosarcoma Cells ◽  
Proliferation And Metastasis ◽  
Induced Apoptosis

The estrogen receptors α (ERα) and β (ERβ) are located in the nucleus and bind to estrogen to initiate transcription of estrogen-responsive genes. In a variety of tumor cells, ERβ has been shown to be a tumor suppressor. In particular, ERβ has anti-proliferative effects in osteosarcoma cells. Additionally, ERβ has been proven to regulate the apoptosis-related molecules IAP, BAX, caspase-3, and PARP, and to act on the NF-κB/BCL-2 pathway to induce apoptosis in tumors. Moreover, ERβ can regulate the expression of the autophagy associated markers LC3-I/LC-3II and p62 and induce autophagy in tumors by inhibiting the PI3K/AKT/mTOR pathway and activating the AMPK pathway. Here, we review the molecular mechanisms by which ERβ induces apoptosis and autophagy in a variety of tumors to further delineate more specific molecular mechanisms underlying osteosarcoma tumorigenesis and pathogenesis. Considering the broad involvement of ERβ in apoptosis, autophagy, and their interaction, it is plausible that the critical role of ERβ in inhibiting the proliferation and metastasis of osteosarcoma cells is closely related to its regulation of apoptosis and autophagy.

Effect of PTH on blood pressure and response to vasoconstrictor agonists

1985 ◽  
Vol 248 (5) ◽  
pp. F674-F681 ◽  
Author(s):  
Y. Saglikes ◽  
S. G. Massry ◽  
K. Iseki ◽  
J. L. Nadler ◽  
V. M. Campese
Keyword(s):  
Blood Pressure ◽  
Inhibitory Effect ◽  
Significant Rise ◽  
Ang Ii ◽  
Vascular Response ◽  
Hypotensive Action ◽  
Amino Terminal ◽  
Before And After ◽  
Hypotensive Response

Parathyroid hormone (PTH) is known to be a vasodilator and to exert a hypotensive action. The present study examined the possible mechanisms involved, with special emphasis on the role of vasodilatory prostaglandins. The effects of the intact 1-84 PTH and that of its amino-terminal 1-34 fragment on mean arterial pressure (MAP) and on the vascular response to norepinephrine (NE) or angiotensin II (ANG II) were examined in rats before and after pretreatment with indomethacin. Bolus injections of 30 U of both 1-84 and 1-34 PTH produced a significant (P less than 0.01) decrease in MAP; however, the hypotensive response to 1-34 PTH (-28 +/- 4.6 mmHg) was more marked (P less than 0.01) than to 1-84 PTH (-9 +/- 1.8 mmHg). The infusion of 1-84 PTH (30 U/h) did not alter MAP, whereas the infusion of 1-34 PTH (30 U/h) led to a decrease in MAP from 124 +/- 2 to 103 +/- 4.0 mmHg (P less than 0.01) and to a rise in heart rate from 359 +/- 30 to 437 +/- 13 beats/min (P less than 0.02). Both 1-84 and 1-34 PTH antagonized the pressor effects produced by bolus injections of NE and ANG II. Pretreatment with indomethacin (5 mg/kg body wt) abolished the inhibitory effect of 1-84 and 1-34 PTH on the response of MAP to NE and ANG II and the hypotensive action of 1-34 PTH. Infusion of 1-84 and 1-34 PTH produced a significant rise in urinary excretion of 6-keto-PGF1 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Molecular Imaging Provides Novel Insights on Estrogen Receptor Activity in Mouse Brain

2008 ◽  
Vol 7 (6) ◽  
pp. 7290.2008.00027 ◽  
Author(s):  
Alessia Stell ◽  
Silvia Belcredito ◽  
Paolo Ciana ◽  
Adriana Maggi
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Transcriptional Activity ◽  
Receptor Activity ◽  
Male And Female ◽  
Estrogen Receptor Activity ◽  
The Central Nervous System ◽  
Set Up

Estrogen receptors have long been known to be expressed in several brain areas in addition to those directly involved in the control of reproductive functions. Investigations in humans and in animal models suggest a strong influence of estrogens on limbic and motor functions, yet the complexity and heterogeneity of neural tissue have limited our approaches to the full understanding of estrogen activity in the central nervous system. The aim of this study was to examine the transcriptional activity of estrogen receptors in the brain of male and female mice. Exploiting the ERE-Luc reporter mouse, we set up a novel, bioluminescence-based technique to study brain estrogen receptor transcriptional activity. Here we show, for the first time, that estrogen receptors are similarly active in male and female brains and that the estrous cycle affects estrogen receptor activity in regions of the central nervous system not known to be associated with reproductive functions. Because of its reproducibility and sensitivity, this novel bioluminescence application stands as a candidate as an innovative methodology for the study and development of drugs targeting brain estrogen receptors.

scholarly journals Role of nitric oxide in hypoxia inhibition of fever

1999 ◽  
Vol 87 (6) ◽  
pp. 2186-2190 ◽  
Author(s):  
Maria C. Almeida ◽  
Evelin C. Carnio ◽  
Luiz G. S. Branco
Keyword(s):  
Nitric Oxide ◽  
Treated Group ◽  
No Production ◽  
Significant Drop ◽  
Before And After ◽  
Synthase Inhibitor ◽  
Dose Dependent ◽  
Concomitant Exposure ◽  
Experimental Group

Hypoxia causes a regulated decrease in body temperature (Tb), and nitric oxide (NO) is now known to participate in hypoxia-induced hypothermia. Hypoxia also inhibits lipopolysaccharide (LPS)-induced fever. We tested the hypothesis that NO may participate in the hypoxia inhibition of fever. The rectal temperature of awake, unrestrained rats was measured before and after injection of LPS, with or without concomitant exposure to hypoxia, in an experimental group treated with N ω-nitro-l-arginine (l-NNA) for 4 consecutive days before the experiment and in a saline-treated group (control).l-NNA is a nonspecific NO synthase inhibitor that blocks NO production. LPS caused a dose-dependent typical biphasic rise in Tb that was completely prevented by hypoxia (7% inspired oxygen).l-NNA caused a significant drop in Tb during days 2–4 of treatment. When LPS was injected intol-NNA-treated rats, inhibition of fever was observed. Moreover, the effect of hypoxia during fever was significantly reduced. The data indicate that the NO pathway plays a role in hypoxia inhibition of fever.

scholarly journals Estrogen Receptors Alpha and Beta Mediate Synaptic Transmission in the PFC and Hippocampus of Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1485
Author(s):  
Mingyue Zhang ◽  
Hannah Weiland ◽  
Michael Schöfbänker ◽  
Weiqi Zhang
Keyword(s):  
Estrogen Receptor ◽  
Synaptic Transmission ◽  
Estrogen Receptors ◽  
Hippocampal Slices ◽  
Physiological Role ◽  
Glutamatergic Transmission ◽  
Postsynaptic Currents ◽  
Specific Manner ◽  
The Brain

Distinct from ovarian estradiol, the steroid hormone 17ß-estradiol (E2) is produced in the brain and is involved in numerous functions, particularly acting as a neurosteroid. However, the physiological role of E2 and the mechanism of its effects are not well known. In hippocampal slices, 17ß-estradiol has been found to cause a modest increase in fast glutamatergic transmission; because some of these effects are rapid and acute, they might be mediated by membrane-associated receptors via nongenomic action. Moreover, activation of membrane estrogen receptors can rapidly modulate neuron function in a sex-specific manner. To further investigate the neurological role of E2, we examined the effect of E2, as an estrogen receptor (ER) agonist, on synaptic transmission in slices of the prefrontal cortex (PFC) and hippocampus in both male and female mice. Whole-cell recordings of spontaneous excitatory postsynaptic currents (sEPSC) in the PFC showed that E2 acts as a neuromodulator in glutamatergic transmission in the PFC in both sexes, but often in a cell-specific manner. The sEPSC amplitude and/or frequency responded to E2 in three ways, namely by significantly increasing, decreasing or having no response. Additional experiments using an agonist selective for ERß, diarylpropionitrile (DPN) showed that in males the sEPSC and spontaneous inhibitory postsynaptic currents sIPSC responses were similar to their E2 responses, but in females the estrogen receptor ß (ERß) agonist DPN did not influence excitatory transmission in the PFC. In contrast, in the hippocampus of both sexes E2 potentiated the gluatmatergic synaptic transmission in a subset of hippocampal cells. These data indicate that activation of E2 targeting probably a estrogen subtypes or different downstream signaling affect synaptic transmission in the brain PFC and hippocampus between males versus females mice.

scholarly journals Role of Estrogen Receptors in Male Reproductive Physiology

2016 ◽  
Vol 3 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Richard R Lee ◽  
Karen P Phillips
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptors ◽  
Intracellular Signaling ◽  
Male Fertility ◽  
Reproductive Tract ◽  
Male Reproduction ◽  
Receptor Subtypes ◽  
G Protein Coupled

Canonical estrogen receptors (ER α/β) have a genomic mechanism of action, functioning as nuclear transcription factors for estrogen-dependent genes. Estrogen receptors are well established within the male reproductive tract with estrogen playing an essential role for male fertility. The recent characterization of novel G-protein coupled estrogen receptor GPR30 (alternatively known as GPER1), depending on non-genomic intracellular signaling pathways to transduce estrogenic signals, requires a re-examination of the roles of estrogen receptors in male reproduction. Further, the affinity of environmental estrogens (xenoestrogens) for estrogen receptor subtypes may provide additional understanding of the reproductive effects of these chemicals on male fertility. Here we review the structure and functions of each estrogen receptor within the context of male reproduction, with special consideration of the reproductive implications of xenoestrogen exposure. 

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