Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENAL CORTEX”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed2002

cAMP-dependent transcription of steroidogenic genes in the human adrenal cortex requires a dual-specificity phosphatase in addition to protein kinase A.

Steroid hormone biosynthesis in the adrenal cortex is controlled by the peptide hormone adrenocorticotropin (ACTH), which acts to increase intracellular cAMP and results in the activation of cAMP-dependent protein kinase A (PKA) and subsequent increase in steroidogenic gene transcription. Protein phosphorylation by PKA activates transcription of genes encoding steroidogenic enzymes; however the precise proteins which are phosphorylated remain to be determined. We have recently shown that phosphoprotein phosphatase (PP) activity is essential for cAMP-dependent transcription of the human CYP17 (hCYP17) gene in H295R adrenocortical cells. The aim of our current studies was to determine if inhibition of PP activity attenuates cAMP-dependent mRNA expression of other steroidogenic genes in H295R cells. Using various inhibitors of serine/threonine and tyrosine PPs, we examined the role of phosphatase activity on cAMP-dependent transcription of steroidogenic genes in the adrenal cortex. CYP11A, CYP11B1/2, CYP21, and adrenodoxin also require PP activity for cAMP-stimulated gene expression. Inhibition of both serine/threonine and tyrosine PP activities suppresses the cAMP-dependent mRNA expression of several steroidogenic genes, suggesting that a dual-specificity PP is essential for conveying ACTH/cAMP-stimulated transcription. We propose that PKA phosphorylates and activates a dual-specificity phosphatase, which mediates steroidogenic gene transcription in response to ACTH/cAMP.

Adrenal Cortex↗
PubMed1991

[Characteristics of the ACTH-adrenal cortex system in women of reproductive age after ovariectomy].

The examination of the function of the ACTH-adrenal cortex system in females of reproductive age following ovariectomy revealed certain hormonal relationships in terms of the clinical course of the disease: in persistent autonomic vascular and psychoemotional disorders there was a reduction or an increase in blood levels of ACTH (depending on the presence or absence of hypertension), cortisol and a decrease in blood testosterone levels, whereas in regression of the disorders there was a decrease in ACTH and cortisol and an elevation of testosterone levels. The development of the postcastration syndrome is likely to depend on the function and response of the ACTH-adrenal cortex system to a definite extent.

Adrenal Cortex↗
PubMed1987

Failure of prostacyclin effect on the reversal of early ultrastructural changes in cell nuclei of adrenal cortex after complete 15-min cerebral ischemia in rabbit.

The experiment was carried out on 18 rabbits in two experimental groups. Group I: animals with complete 15-min cerebral ischemia infused with PGI2 for 3 min before, during and for 15-min after ischemia. Group II = control: animals with complete 15 min cerebral ischemia. In both groups, cell nuclei of the adrenal cortex were examined. In the 3rd and 6th h after ischemia numerous vesicular structures, intranuclear filaments and granulofibrillar bodies were found in the nuclei. The vesicular structures were enclosed in a single smooth membrane, some combined with the nuclear envelope, others remained independent. Amassing in karyoplasm of vesicular structures, intranuclear filaments and granulofibrillar bodies probably leads to death of the adrenal cortex cell after complete cerebral ischemia. It is suggested that vesicular structures may form as the result of disturbances in the water-electrolyte exchange between cytoplasm and karyoplasm of adrenal cells. In the experimental conditions, PGI2 did not affect the development of irreversible ultrastructural changes in adrenal cortex cell nuclei after complete prolonged cerebral ischemia.

Adrenal Cortex↗
PubMed2001

Immunoelectron microscopic localization of three key steroidogenic enzymes (cytochrome P450(scc), 3 beta-hydroxysteroid dehydrogenase and cytochrome P450(c17)) in rat adrenal cortex and gonads.

The biosynthesis of steroid hormones in endocrine steroid-secreting glands results from a series of successive steps involving both cytochrome P450 enzymes, which are mixed-function oxidases, and steroid dehydrogenases. So far, the subcellular distribution of steroidogenic enzymes has been mostly studied following subcellular fractionation, performed in placenta and adrenal cortex. In order to determine in situ the intracellular distribution of some steroidogenic enzymes, we have investigated the ultrastructural localization of the three key enzymes: P450 side chain cleavage (scc) which converts cholesterol to pregnenolone; 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) which catalyzes the conversion of 3 beta-hydroxy-5-ene steroids to 3-oxo-4-ene steroids (progesterone and androstenedione); and P450(c17) which is responsible for the transformation of C(21) into C(19) steroids (dehydroepiandrosterone and androstenedione). Immunogold labeling was used to localize the enzymes in rat adrenal cortex and gonads. The tissues were fixed in 1% glutaraldehyde and 3% paraformaldehyde and included in LR gold resin. In the adrenal cortex, both P450(scc) and 3 beta-HSD immunoreactivities were detected in the reticular, fascicular and glomerular zones. P450(scc) was exclusively found in large mitochondria. In contrast, 3 beta-HSD antigenic sites were mostly observed in the endoplasmic reticulum (ER) with some gold particles overlying crista and outer membranes of the mitochondria. P450(c17) could not be detected in adrenocortical cells. In the testis, the three enzymes were only found in Leydig cells. Immunolabeling for P450(scc) and 3 beta-HSD was restricted to mitochondria, while P450(c17) immunoreactivity was exclusively observed in ER. In the ovary, P450(scc) and 3 beta-HSD immunoreactivities were found in granulosa, theca interna and corpus luteum cells. The subcellular localization of the two enzymes was very similar to that observed in adrenocortical cells. P450(c17) could also be detected in theca interna cells of large developing and mature follicles. As observed in Leydig cells, P450(c17) immunolabeling could only be found in the ER. These results indicate that in different endocrine steroid-secreting cells P450(scc), 3 beta-HSD and P450(c17) have the same association with cytoplasmic organelles (with the exception of 3 beta-HSD in Leydig cells), suggesting similar intracellular pathways for biosynthesis of steroid hormones.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

Effects of testosterone on the zona fasciculata of the male rat adrenal cortex. A correlated stereological and biochemical study.

The effects of long-term testosterone administration on the adrenal cortex of male rats were investigated by coupled morphometric and biochemical methods. Morphometry showed that testosterone treatment provoked a time-dependent atrophy of the zona fasciculata cells, which was mainly due to the decrease in the volume of the mitochondrial compartment and smooth endoplasmic reticulum (SER). Biochemical assays demonstrated that the decrease in the surface area per cell of SER membranes and mitochondrial cristae was tightly paralleled by the decrease in the activity per cell of two key enzymes of steroid synthesis contained in them (delta 5-3 beta-hydroxysteroid dehydrogenase and 11 beta-hydroxylase). The testosterone-induced inhibition of the growth maintenance and steroidogenic capacity of adrenocortical cells provoked a significant fall in the plasma concentration of corticosterone and a consequential increase in the level of circulating ACTH. Chronic administration of testosterone caused a notable suppression of the activity of the adrenal 5 alpha-reductase and this in turn provoked a rise in the intracellular concentration of corticosterone. Moreover, testosterone inhibited the incorporation of 3H-uridine into the nuclear and mitochondrial fractions of male rat adrenocortical cells. These findings exclude the possibility that the testosterone-provoked atrophy of the male rat adrenal glands is mediated by the suppression of the hypothalamo-hypophyseal axis, and suggest that the mechanism underlying this action of testosterone involves inhibition of nuclear and mitochondrial RNA synthesis. Whether this effect of testosterone is directly or indirectly mediated by the rise in the intracellular content of corticosterone due to the inhibition of 5 alpha-reductase activity, remains to be elucidated.

3-Hydroxysteroid Dehydrogenases↗
PubMed2005

Differential expression and function of beacon in the rat adrenal cortex and medulla.

Beacon gene is overexpressed in obese rats, and beacon was found to stimulate food intake. Evidence has been recently provided that beacon is also expressed in the endocrine glands of normal rats, including adrenal cortex, of which it appears to regulate secretory activity. To further characterize the role of beacon in the rat adrenals, we investigated the level of beacon expression in the adrenal zona glomerulosa (ZG), zona fasciculata-reticularis (ZF/R) and medulla (AM), and the in vitro secretory responses to beacon[47-73] (hereinafter, beacon) of adrenocortical and adrenomedullary tissues. Real-time polymerase chain reaction revealed similar high levels of beacon mRNA in the ZG and ZF/R, and significantly lower (-80%) levels in AM. Immunocytochemistry showed that the distribution of beacon protein followed that of beacon mRNA. Quantitative high pressure liquid chromatography demonstrated that beacon (5x10(-7) M) reduced by about 56% the in vitro total steroid-hormone production from ZG and ZF/R tissues, without affecting catecholamine secretion from AM specimens. The beacon-induced lowering in the secretory activity of adrenal cortex depended on similar reductions (from 50-64%) in the production of the main adrenocortical hormones (pregnenolone, progesterone, 11-deoxycorticosterone, corticosterone, 18-hydroxy-corticosterone and aldosterone), thereby suggesting an inhibitory action of beacon in the early step of steroidogenesis (i.e. the conversion of cholesterol to pregnenolone). The hypothesis is advanced that beacon is to be considered an autocrine-paracrine negative regulator of mineralo- and glucocorticoid synthesis in the rat adrenal gland.

Adrenal Cortex↗
PubMed1997

Correlation of mast cells with spindle cell hyperplasia in the adrenal cortex of IQI/Jic mice.

IQI/Jic mice showed a high incidence of subcapsular spindle cell hyperplasia (SCH) in the adrenal cortex accompanied by prominent mast cell infiltration. SCH-positive animals appeared as early as at 3 months of age, with an incidence of 18% in males and 20% in females. Except for one mouse, all females older than 6 months had the lesion. In males, the incidence increased gradually until 9 months, and was then stable at 75-88% thereafter. The severity of SCH increased with age in both sexes, and the lesions were more prominent in females. Mast cells infiltrated mainly at the sites of spindle cell hyperplasia, and their density was associated with the severity on the lesion. A quantitative morphometric study confirmed a significant correlation between the severity of SCH and the density of mast cells. A histochemical study demonstrated that these mast cells were of the connective tissue-type. These observations indicate that IQI/Jic mice may be a useful strain to elucidate the pathogenesis of SCH in the adrenal cortex in association with mast cell function.

Adrenal Cortex↗