Modulation of plasminogen activation by glucocorticoid hormones in the rat granulosa cell

Harlow, Christopher R.; Coombs, R. J.; Hodges, J. K.; Jenkins, Nigel

doi:10.1677/joe.0.1140207

Cited by 13 publications

(3 citation statements)

References 9 publications

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“…The treatment groups were as follows: control [phosphate-buffered saline (PBS) only]; vehicle control (0.1% ethanol); phenytoin, a positive control for neural tube defects (Fisher Scientific); iAs as sodium arsenite (iAs 3+ ; Sigma-Aldrich, St. Louis, MO); cortexolone, a GR inhibitor (Fisher Scientific); phenytoin plus cortexolone; and iAs 3+ plus cortexolone. We selected the concentration of cortexolone on the basis of previous studies (Harlow et al 1987; Turnell et al 1974). …”

Section: Methodsmentioning

confidence: 99%

Systems Biology and Birth Defects Prevention: Blockade of the Glucocorticoid Receptor Prevents Arsenic-Induced Birth Defects

Ahir

Sanders

Rager

et al. 2013

Environ Health Perspect

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Background: The biological mechanisms by which environmental metals are associated with birth defects are largely unknown. Systems biology–based approaches may help to identify key pathways that mediate metal-induced birth defects as well as potential targets for prevention.Objectives: First, we applied a novel computational approach to identify a prioritized biological pathway that associates metals with birth defects. Second, in a laboratory setting, we sought to determine whether inhibition of the identified pathway prevents developmental defects.Methods: Seven environmental metals were selected for inclusion in the computational analysis: arsenic, cadmium, chromium, lead, mercury, nickel, and selenium. We used an in silico strategy to predict genes and pathways associated with both metal exposure and developmental defects. The most significant pathway was identified and tested using an in ovo whole chick embryo culture assay. We further evaluated the role of the pathway as a mediator of metal-induced toxicity using the in vitro midbrain micromass culture assay.Results: The glucocorticoid receptor pathway was computationally predicted to be a key mediator of multiple metal-induced birth defects. In the chick embryo model, structural malformations induced by inorganic arsenic (iAs) were prevented when signaling of the glucocorticoid receptor pathway was inhibited. Further, glucocorticoid receptor inhibition demonstrated partial to complete protection from both iAs- and cadmium-induced neurodevelopmental toxicity in vitro.Conclusions: Our findings highlight a novel approach to computationally identify a targeted biological pathway for examining birth defects prevention.

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Section: Methodsmentioning

confidence: 99%

Systems Biology and Birth Defects Prevention: Blockade of the Glucocorticoid Receptor Prevents Arsenic-Induced Birth Defects

Ahir

Sanders

Rager

et al. 2013

Environ Health Perspect

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“…Several species 11 , 12 require glucocorticoids for complete oocyte maturation and cortisol specifically antagonizes the effect of follicle stimulating hormone (FSH) in cultured murine granulosa‐lutein cells through the inhibition of plasminogen activator, a protein directly involved in ovulation 13 . An important role for cortisol in human ovarian function has been suggested 14 .…”

Section: Introductionmentioning

confidence: 99%

Total Cortisol Levels are Reduced in the Periovulatory Follicle of Infertile Women with Minimal–Mild Endometriosis

Smith

Keay

Margo

et al. 2002

American J Rep Immunol

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“…For example, corticosterone and dexamethasone suppressed plasminogen activator production (Harlow et al, 1987) and at high concentrations reduced the induction of LH receptors and aromatase activity by FSH but enhanced FSH-stimulated progesterone secretion (Hsueh & Erickson, 1978;Adashi et al, 1981;Schoonmaker & Erickson, 1983).…”

Section: Introductionmentioning

confidence: 99%

Enhanced secretion of oxytocin from bovine granulosa cells treated with adrenal steroids

Lück¹

1988

Reproduction

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Bovine granulosa cells were exposed in vitro to various adrenal steroids (cortisol, cortisone, corticosterone, aldosterone; 1 mumol/l), in the presence and absence of stimulation by ascorbic acid (0.5 mmol/l), to determine the possible effects of these hormones on ovarian oxytocin and progesterone secretion. Only cortisol produced a consistent stimulation of the cells; the response was dose-related over the range 0.01 to 1.0 mumol/l and was greatly enhanced in the presence of ascorbate. The secretion of oxytocin was stimulated to a greater extent and with more consistency than was that of progesterone. Although the secretion of oxytocin could be stimulated by cortisol on the day of treatment, the cells also showed a delayed and persistent response to exposure earlier in the culture. It is concluded that cortisol may directly stimulate the secretion of ovarian oxytocin in the cow and that granulosa cells may respond in such a way as to smooth out the effects of short-term fluctuations in cortisol concentration.

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Modulation of plasminogen activation by glucocorticoid hormones in the rat granulosa cell

Cited by 13 publications

References 9 publications

Systems Biology and Birth Defects Prevention: Blockade of the Glucocorticoid Receptor Prevents Arsenic-Induced Birth Defects

Systems Biology and Birth Defects Prevention: Blockade of the Glucocorticoid Receptor Prevents Arsenic-Induced Birth Defects

Total Cortisol Levels are Reduced in the Periovulatory Follicle of Infertile Women with Minimal–Mild Endometriosis

Enhanced secretion of oxytocin from bovine granulosa cells treated with adrenal steroids

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