Estrogen-induced protein. Time course of synthesis

Barnea, Ayalla; Gorski, Jack

doi:10.1021/bi00811a006

Cited by 131 publications

(35 citation statements)

References 3 publications

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“…These mechanisms involve the binding of estrogen-response elements to target genes, or protein-protein interaction subsequently modifying transcription. The time necessary for new protein synthesis is ϳ30 -45 min, and probably an even much longer time is required to alter cellular physiology (1). It is unlikely, therefore, that the effects of estrogen seen in our study were caused by the activation of a genomic mechanism.…”

Section: Discussionmentioning

confidence: 77%

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Schmitt¹,

Kaufman²

2005

Journal of Applied Physiology

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Schmitt, Petra M., and Marc P. Kaufman. Estrogen's attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats. J Appl Physiol 98: 633-639, 2005. First published September 24, 2004 doi:10.1152/ japplphysiol.00788.2004.-Using gonadally intact female cats, we showed previously that estrogen, applied topically to the spinal cord, attenuated the exercise pressor reflex. Although the mechanism by which estrogen exerted its attenuating effect is unknown, this steroid hormone has been shown to influence spinal opioid pathways, which in turn have been implicated in the regulation of the exercise pressor reflex. These findings prompted us to test the hypothesis that opioids mediate the attenuating effect of estrogen on the exercise pressor reflex in both gonadally intact female and ovariectomized cats. We therefore applied 200 l of 17␤-estradiol (0.01 g/ml) with and without the addition of 1,000 g naloxone, a -and ␦-opioid antagonist, to a spinal well covering the L 6-S1 spinal cord in decerebrated female cats that were either gonadally intact or ovariectomized. The exercise pressor reflex was evoked by electrical stimulation of the L 7 or S1 ventral root, a maneuver that caused the hindlimb muscles to contract statically. We found that, in gonadally intact cats, the attenuating effect of estrogen was more pronounced than that in ovariectomized cats. We also found that, in gonadally intact female cats, naloxone partly reversed the attenuation of the pressor response to static contraction caused by spinal estrogen application. For example, in intact cats, the pressor response to contraction before estrogen application averaged 39 Ϯ 4 mmHg (n ϭ 10), whereas the pressor response 60 min afterward averaged only 18 Ϯ 4 mmHg (P Ͻ 0.05). In contrast, the pressor response to contraction before estrogen and naloxone application averaged 33 Ϯ 5 mmHg (n ϭ 11), whereas afterward it averaged 27 Ϯ 6 mmHg (P Ͻ 0.05). In ovariectomized cats, naloxone was less effective in reversing the attenuating effect of estrogen on the exercise pressor reflex. sex hormones; static contraction; blood pressure; neural control of circulation; autonomic nervous system THE EXERCISE PRESSOR REFLEX consists of increases in mean arterial pressure, heart rate and ventilation that are evoked by static contraction of the hindlimb muscles in anesthetized or decerebrated animals (19). Recently, spinally applied estrogen was found to attenuate the arterial pressure component of the exercise pressor reflex in decerebrated cats. This attenuation was shown to be gender specific because the threshold concentration of estrogen needed to attenuate the pressor response to contraction was 1,000 times more dilute in female cats than it was in male cats (24,25).The mechanism by which spinally applied estrogen attenuated the reflex pressor response to static contraction is unknown. Nevertheless, -opioid receptors and ␦-opioid receptors have been implicated in the spinal regulation of the exercise pressor ...

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Section: Discussionmentioning

confidence: 77%

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Schmitt¹,

Kaufman²

2005

Journal of Applied Physiology

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“…The classical mechanism of estrogen action is for E2 to bind to intracellular ERs, which form dimers, bind to EREs, and directly regulate transcription of estrogen-sensitive genes. These transcriptional, or "genomic," events have long been thought to take hours to days (Barnea and Gorski, 1970). However, rapid effects of E2 have been described.…”

Section: Discussionmentioning

confidence: 99%

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Temple¹,

Laing²,

Sunder³

et al. 2004

J. Neurosci.

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Pulsatile secretion of gonadotropin-releasing hormone-1 (GnRH-1) is essential for reproduction. GnRH-1 induces gonadotropin release and is regulated by 17␤-estradiol (E2). Although a subpopulation of GnRH-1 neurons expresses estrogen receptor (ER) ␤, it is unclear whether E2 acts directly on GnRH-1 neurons or indirectly through interneuronal connections. To test the hypothesis that E2 acts directly on GnRH-1 neurons to regulate neuronal activity, we used calcium imaging to monitor intracellular calcium oscillations in GnRH-1 neurons maintained in nasal explants. TTX was used to minimize synaptic input from other cells. Consistent with previous studies, TTX reduced the activity of individual GnRH-1 neurons to a basal level, while the population of cells maintained synchronized calcium oscillations. Exposure of GnRH-1 cells to TTX plus E2 increased the number of calcium peaks/cell, percentage of cells with Ն10 peaks, mean peak amplitude, and percentage of cells that contributed to each calcium pulse in explants maintained in vitro for 7 d (7 div) compared with TTX alone. These effects were induced within 30 min and were not mimicked by 17␣-estradiol, E2 conjugated to BSA (which does not cross the plasma membrane), or seen at 21 div, when the percentage of GnRH-1 cells expressing ER␤ transcripts declines. In addition, these effects were inhibited by the ER antagonist ICI 182,780 and prevented by inhibition of gene transcription. These data suggest that, via ER␤, E2 can rapidly act as a hormone-activated transcription complex and are the first to show that E2 directly increases GnRH-1 neuronal activity and synchronization.

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“…Not only do they maintain general metabolic processes, they also induce synthesis of "specific proteins" and structural differentiation in normal target cells (Kohler et al, 1967;O'Malley et al, 1969;Gorski and Notides, 1969;Barnea and Gorski, 1970;DeAngelo and Gorski, 1970), and maintain growth and proliferation in estrogendependent malignant tissues (Huggins et al, 1959). Specific protein synthesis precedes general protein synthesis (Hamilton, 1968), increment in cytoplasmic mass, and cellular proliferation.…”

Section: Discussionmentioning

confidence: 99%

Endogenous peroxidase: specific marker enzyme for tissues displaying growth dependency on estrogen.

Anderson¹,

Kang²,

DeSombre³

1975

The Journal of Cell Biology

106

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Data derived from a correlated morphological and biochemical study suggest the following: (a) estradiol-17~, diethylstilbestrol, the estrogen antagonists nafoxidine (Upjohn 11,100), and Parke Davis CI628 induce synthesis of an endogenous peroxidase in the epithelium of target tissues like the vagina, the cervix, the uterus, and in the acinar cells of the estrogen-dependent rat mammary tumor; (b) peroxidase is a "specific" secretory protein of the estrogen-sensitized uterine endometrium; (c) peroxidase synthesis is not a nonspecific response to steroid hormone action, since progesterone and testosterone do not induce its synthesis; (d) endogenous peroxidase is a possible diagnostic protein for the detection of estrogen-dependent growing tissues, including breast cancer; (e) movement of exogenous horseradish peroxidase from the interstitium to the uterine lumina is restricted by tight junctions located at the apices of epithelial cells. Estrogen and antagonists do not appear to influence the transepithelial movement of exogenous peroxidase into the lumen.The uterus, cervix, vagina, and mammary gland of mammals require estrogen for their postpubertal trophic development and for the maintenance of their differentiated state. Indeed, the presence of estrogen-binding proteins (estrogen receptors or estrophiles, Jensen et al., 1966 a) in these tissues and of estrogen dependency of rat and human mammary carcinoma are well documented (Huggins et al., 1959; Jensen et al., 1966 b;Heuson et al., 1972).In the course of our investigation it was discovered that tissues displaying growth dependency on estrogen synthesize and secrete "specific marker proteins" into their lumina. These results show (a) that synthesis of peroxidase ~ (or a hemoprotein with peroxidatic activity) is a consistent marker for estrogen-dependent tissues (carcinogen-induced rat mammary carcinoma, cervix, vagina, and uterus), (b) estrogen antagonists (Upjohn 11,100; ~Throughout this paper, the DAB-positive reaction product will be referred to as peroxidase, since uterine peroxidase is a well-documented enzyme (see text) and since the histochemical medium employed is designed to demonstrate peroxidase activity. It is of course possible that what is being visualized in either a hemeprotein, which may possess peroxidase activity, or several substances with peroxidasic activity. The biochemical characterization of this enzyme as a peroxidase is still very limited.

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Estrogen-induced protein. Time course of synthesis

Cited by 131 publications

References 3 publications

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Estrogen’s attenuating effect on the exercise pressor reflex is more opioid dependent in gonadally intact than in ovariectomized female cats

Direct Action of Estradiol on Gonadotropin-Releasing Hormone-1 Neuronal Activity via a Transcription-Dependent Mechanism

Endogenous peroxidase: specific marker enzyme for tissues displaying growth dependency on estrogen.

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