Effect of 5α-dihydrotestosterone and dexamethasone on estrogen receptors of the anterior pituitary and uterus

Zamorano, Pedro; Steinsapir, Jaime; Mahesh, Virendra B.

doi:10.1016/0039-128x(92)90091-m

Cited by 14 publications

(7 citation statements)

References 37 publications

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“…In that study there appeared to be no changes in -actin mRNA levels at different times after estradiol administration, and the results were similar whether they were corrected using -actin or uncorrected for variations in transfer. Other tissue-specific differences in ER dynamics between the pituitary and the uterus have been reported by us earlier using progesterone [11,46], 5oL-pregnane-3,20-dione [22], and a5o-dihydrotestosterone and dexamethasone [16]. Furthermore, in the present study, ER mRNA levels in the uterus were increased after ovariectomy and decreased after estrogen priming, whereas in the anterior pituitary ER mRNA levels are decreased after ovariectomy and increased after estrogen priming [45].…”

Section: Discussionsupporting

confidence: 42%

“…ER binding was performed according to Zamorano et al [16]. Briefly, uteri were placed in cold homogenization buffer (TEDSP: 10 mM Tris-HCI, 1.5 mM EDTA, 1.0 mM dithiothreitol [DTT], 250 mM sucrose, and 1 mM PMSF, pH 7.4) and homogenized in a Polytron PT 10 (Polysciences, Inc., Warrington, PA) with three 15-sec bursts at setting #5 with cooling for 15 sec on ice between each burst.…”

Section: Measurement Of Er Bindingmentioning

confidence: 99%

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Changes in Rat Uterine Estrogen Receptor Messenger Ribonucleic Acid Levels during Estrogen- and Progesterone-Induced Estrogen Receptor Depletion and Subsequent Replenishment1

Rosser

Chorich

Howard

et al. 1993

Biology of Reproduction

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The overall objectives of this study were to determine whether the rapid decrease in estrogen receptor (ER) binding in the rat uterus after an injection of estradiol and subsequent recovery of ER levels was accompanied by similar changes in ER mRNA levels. Furthermore, the effect of progesterone administered under conditions known to decrease ER binding, in the rat uterus, on ER mRNA levels was also investigated. Ovariectomy for 14 days brought about a 3-fold increase in rat uterine ER mRNA levels, and these elevated levels were decreased by a 3-day treatment with 2 micrograms of estradiol in ethanol/saline injected i.p. In the ovariectomized rat, 1 and 5 micrograms of estradiol brought about small but significant decreases in ER mRNA levels in 1 h, which did not parallel the rapid decrease in ER binding at that time reported earlier. The 10-micrograms dose of estradiol brought about a bigger decrease in ER mRNA levels. In the ovariectomized rat primed with estradiol (2 micrograms/day in ethanol/saline), the administration of 2 micrograms of estradiol brought about no change in uterine ER mRNA levels at 6 h as compared to the 1-h time point if the values were not corrected for beta-actin, which was significantly increased at 6 h. A dramatic increase in ER mRNA levels 12 h after the estradiol injection preceded the increase in ER binding observed at 18 h. Progesterone (0.8 mg/kg body weight [BW]) in the absence of estrogen priming brought about minimal but significant inhibition of ER mRNA levels 12 and 18 h after administration, with no effects at 1 and 6 h. In the presence of estrogen priming, the 0.8-mg/kg BW dose of progesterone did not cause any changes in ER mRNA levels beyond those brought about by estrogen alone after 1 h, even though it has been shown to significantly decrease ER binding. This was also true when a larger dose of progesterone (2.0 mg/kg BW) was used, a dose that decreases ER binding to a significantly greater extent than the 0.8-mg/kg BW dose. However, the 4.0-mg/kg BW dose of progesterone decreased ER mRNA levels. Thus a single injection of estradiol appears to cause a decrease in ER binding primarily by accelerated receptor processing and degradation with small changes in ER mRNA within the first hour. A significant increase in uterine ER mRNA at 12 h precedes increased ER binding at 18 h. This indicates new synthesis of ER during the recovery period.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Discussionsupporting

confidence: 42%

Section: Measurement Of Er Bindingmentioning

confidence: 99%

Changes in Rat Uterine Estrogen Receptor Messenger Ribonucleic Acid Levels during Estrogen- and Progesterone-Induced Estrogen Receptor Depletion and Subsequent Replenishment1

Rosser

Chorich

Howard

et al. 1993

Biology of Reproduction

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“…Hence, differences between the effect of daily and weekly administration of ACTH on uterine histology and cell proliferation may be due to changes in the expression of oestrogen receptor α. This contention is supported by previous data that showed a decrease in oestrogen receptor content in the uterus after treatment with glucocorticoids (Atkinson and Adams, 1988;Zamorano et al, 1992). The effects of ACTH on all parameters tested were seen only in oestrogen-treated mice and were not observed in control animals that received olive oil in place of oestradiol, which indicates that ACTH affects the mechanism of oestrogen action.…”

Section: Discussionsupporting

confidence: 83%

Effect of adrenocorticotrophic hormone on the development of oestrogen-induced changes and hyperplasia formation in the mouse uterus

Gunin¹

2002

Reproduction

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“…Direct effect of increased level of glucocorticoids over ovaries results atresia of follicles (Meurer et al, 1991). Increased level of Glucocorticoids also have role in expression of estrogen receptors (Zamorano et al, 1992), tissue uptake of estrogen and estrogen stimulated DNA synthesis in uterus (Bigsby, 1993). Levels of synthesis of estrogen get reduced by the inhibitory effect of glucocorticoids over granulosa cell aromatase activity (Hsueh and Erickson, 1978).…”

Section: Effect Of Stress On Hpo Axis Via Crh Acth and Glucocorticoidsmentioning

confidence: 99%

Stress and fertility-Past conviction, present cognizance and future orchestrations

Sarita

Byadgi

S.P

2019

ijrps

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Different studies have been done to study the effect of stress on reproductive physiology and fertility. Pathogenesis of stress-induced infertility /decrease fecundity is explained by various neuro-hormonal axis and theory of oxidative stress, but proper management of stress and regulation of these neurohormonal axis along with oxidative stress is lacking in modern medical science. A better understanding of stress and its relation with body physiology, especially fertility, is attempted in light of Ayurveda to get knowledge about the etiopathogenesis of stress-induced infertility and its holistic management. In Ayurveda concept of stress is not only con ined to psychological factors, but it is the state of disturb body homeostasis, i.e. the state where doshas, dhatus, malas &agni are not in their proper functioning. Diet and lifestyle have their role in maintaining body homeostasis. Along with diet and lifestyle various drugs, therapeutic procedure (panchakarma) & non-materialistic treatment (achar rasayan-rules and beliefs to be followed in life) have been described in Ayurveda to manage disturbed body homeostasis, and thus it helps in the management of stress in a holistic way. Concept of stress management by Ayurvedic concepts like diet, lifestyle, Agni, body puri ication methods along with rasayan and ojo-vardhak objects (diet, lifestyle, and drugs) will open a vast area of research about the applicability of these concepts in stress management by the holistic way. It will help to serve society by providing not only cure of stress-related infertility but also give a healthy reproductive life.

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Effect of 5α-dihydrotestosterone and dexamethasone on estrogen receptors of the anterior pituitary and uterus

Cited by 14 publications

References 37 publications

Changes in Rat Uterine Estrogen Receptor Messenger Ribonucleic Acid Levels during Estrogen- and Progesterone-Induced Estrogen Receptor Depletion and Subsequent Replenishment1

Changes in Rat Uterine Estrogen Receptor Messenger Ribonucleic Acid Levels during Estrogen- and Progesterone-Induced Estrogen Receptor Depletion and Subsequent Replenishment1

Effect of adrenocorticotrophic hormone on the development of oestrogen-induced changes and hyperplasia formation in the mouse uterus

Stress and fertility-Past conviction, present cognizance and future orchestrations

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