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PubMedDate not supplied

Hormonally regulated components of the adrenocortical cell environment and the control of adrenal cortex homeostasis.

The extracellular matrix (ECM) strongly contributes to the regulation of cell proliferation and cell differentiation, and thereby of embryonic development and adult tissue homeostasis. We review here the ongoing characterization of the structure and functions of the extracellular matrix components secreted by adrenocortical cells and discuss their possible implication in the hormonal regulation of adrenal cortex homeostasis. Fibronectin (FN) and laminin (LN) are both major adhesive proteins for adrenocortical cells. FN is synthesized by bovine fasciculata cells in primary culture, and its synthesis is stimulated by TGF(beta)1, TGF(beta)2, and FGF-2 but is not modified by IGF-1 or by the hormones ACTH and angiotensin II. LN is also synthesized by bovine fasciculata cells and its synthesis is specifically stimulated by ACTH. Both proteins are haptotactic and chemotactic for adrenocortical cells, suggesting a physiological role in adrenocyte migration. Their distribution in the adrenal gland is quite distinct. LN is uniformly present in the steroidogenic cells from the three zones, whereas FN is abundant in the fibrovascular structures of the capsule and the cortex. ACTH treatment of adrenocortical cells strongly induces the expression and secretion of thrombospondin-2 (TSP2), a large trimeric matricellular protein. The multimodular structure of TSP2 is the support of a variety of biological functions. TSP2 promotes attachment but prevents spreading of adrenocortical cells. On the other hand, TSP2 induces the activation of latent TGFbeta through an indirect mechanism and is anti-angiogenic in vitro. The overall distribution of TSP2 in the glomerulosa and fasciculata zones of the adrenal cortex, and its absence from the reticularis zone, argue in favor of a role in the protection of adrenocortical cells against apoptosis. In the adrenal cortex, five main biological functions are potentially regulated by components of the extracellular matrix : stem cell commitment into the adrenocyte differentiation pathway, terminal differentiation toward the three distinct adrenocyte phenotypes, centripetal migration, apoptosis and the formation of the capillary network. Future studies will aim at deciphering which extracellular component(s) is involved in each of these regulations.

Adrenal Cortex↗
PubMed1990

Long-term effects of neuropeptide-Y on the rat adrenal cortex.

Adult female rats, intact or dexamethasone suppressed, were i.p. injected twice a day for 4 consecutive days with 0.5 ug neuropeptide-Y (NPY). In intact rats, NPY lowered serum ACTH and aldosterone levels, and had no effects either on serum and adrenal corticosterone or the morphology of the adrenal cortex. In dexamethasone-treated rats, NPY again decreased serum aldosterone concentration. Moreover, it caused a small but significant drop both in the volume of zona fasciculata cells and the adrenal content of corticosterone. These findings seem to suggest an inhibitory effect of NPY on the function of rat zona glomerulosa and perhaps zona fasciculata.

Adrenal Cortex↗
PubMedDate not supplied

[Isolation, purification and study of the properties of pyruvate kinase from the bovine adrenal cortex].

Pyruvate kinase (ATP: pyruvate 2-0-phosphotransferase, EC 2. 7. 1. 40) from bovine adrenal cortex was purified 243 fold. The whole purification procedure included ammonium sulphate fractionation, heat treatment, Sephadex HW-55 chromatography and phosphocellulose chromatography. The specific activity of the preparation is 15.6 U/mg at 30 degrees C, the yield--36%. Pyruvate kinase showed only one protein band as judged by sodium dodecyl sulphate acrylamide gel electrophoresis. The enzyme displayed a hyperbolic saturation curve with respect to P-enolpyruvate. The apparent Km for this substrate was 0.55 X 10(-4) M, pH optimum--6.8-7.0. K+ concentrations above 0.1 M inhibit the enzyme.

Adrenal Cortex↗
PubMed1986

Cyclic AMP-dependent protein kinase activity and protein phosphorylation in zones of the adrenal cortex.

Steroidogenesis is not stimulated by ACTH in the inner zone of the guinea pig adrenal cortex; adenylate cyclase is normally stimulated. To further explore the lack of a steroidogenic response to ACTH in the inner zone, cAMP-dependent protein kinase activity and protein phosphorylation were examined in the outer and inner adrenocortical zones. To summarize: total cAMP-dependent protein kinase activity was 40% higher in the outer zone than in the inner zone; of the total cAMP-dependent protein kinase activity, cytosol contained 80% for the outer and 70% for the inner zone. In both zones only the type II isozyme was present. Qualitative and quantitative differences in protein phosphorylation were noted for the two zones.

Adrenal Cortex↗
PubMedDate not supplied

Expression of ACTH receptors (MC2-R and MC5-R) in the glomerulosa and the fasciculata-reticularis zones of bovine adrenal cortex.

The recent cloning of a family of melanocortin receptors (MC-R) has identified five distinct G protein- and adenylate cyclase-coupled receptors. The MC2-receptor (MC2-R) preferentially binds ACTH. It is expressed in the adrenal cortex and is hence considered to be the ACTH receptor. The MC5-receptor (MC5-R) binds ACTH and alpha-MSH and is more widely expressed. The aim of this work was to study the sites of MC5-R expression in the bovine adrenal cortex and to compare the regulation of the expression of MC2-R and MC5-R in bovine adrenocortical cells in primary culture. Analysis of the expression of MC5-R was obtained by RT-PCR, using total RNA purified from glomerulosa and fasciculata zones of bovine adrenocortical tissue. MC5-R expression could be detected in RNA from the glomerulosa zone but was undetectable in the fasciculata zone. In bovine adrenocortical cells in culture, ACTH stimulates MC5-R expression in the glomerulosa and fasciculata cells. A DNA fragment, was obtained using primers based on the bovine ACTH receptor (MC2-R) sequence. This fragment was detected in RNA from the two zones. The probe was used to quantify MC2-R by Ribonuclease Protection assay and we observed that MC2-R mRNA is 3.6-fold more abundant in glomerulosa than in fasciculata-reticularis cells.

Adrenocorticotropic Hormone↗
PubMed1986

An abnormal response of the adrenal cortex to insulin: glucose in essential hypertension.

This investigation demonstrates an abnormal response to the adrenal cortex to modulation of the potassium metabolism by an intravenous infusion of insulin-glucose in patients with essential hypertension. In response to insulin-glucose there was a transient decline of plasma aldosterone and plasma cortisol concentrations in control subjects with normal blood pressure, whereas a temporary increase of both hormones was found in patients with essential hypertension. Treatment with thiazide diuretics further magnified the different aldosterone response between the two groups. It is suggested that the abnormal response of patients with essential hypertension may be of significance to the understanding of the pathogenesis of this important disease.

Adrenal Cortex↗
PubMed1987

The human adrenal cortex: ultrastructure and base-line morphometric data.

The morphology of the human adult female adrenal cortex was studied by electron microscopy and morphometry. Zona glomerulosa contains outer undifferentiated small cells and inner well-differentiated larger elements, which display mitochondria with tubulo-laminar cristae, abundant smooth endoplasmic reticulum (SER) and sparse lipid droplets. Zona fasciculata cells possess typical mitochondria with vesicular cristae, a well-developed SER, lipid droplets and some lipofuscin-pigment granules, which increase in number in the cells of the inner portion of the zone. Sometimes lipid-laden cells can be observed in the zona fasciculata. Zona reticularis cells have the same morphological features as the zona fasciculata elements, but display a striking rise in the number of lipofuscin-pigment granules.

Adrenal Cortex↗
PubMed1994

Cloning of ACTH-regulated genes in the adrenal cortex.

To search for genes that are induced by ACTH in adrenocortical cells, we screened adrenal cortex cDNA libraries by a differential hybridization method using cDNA probes representing mRNAs from cells with or without ACTH stimulation. Forty clones were identified as ACTH induced (yielding a frequency of about 1/2500 plaques screened), and two clones as ACTH repressed. The cDNAs isolated and sequenced include nuclear genes for microsomal steroidogenic enzymes and novel proteins of yet unidentified functions, and mitochondrial genes encoding subunits of oxidative phosphorylation enzymes. Northern blot analysis of RNA from cells stimulated with ACTH confirmed the induction of these genes by ACTH, yet revealed important differences in the relative responses of the respective mRNAs. The time courses showed the major increase in the initial 6 h; and a decline after 24-36 h. The enhancement of the levels of the mRNAs could be ascribed to transcriptional activation. Since the mitochondrial genome is transcribed as a single polycistronic unit, to account for the > 20-fold differences in the levels of the mitochondrial mRNAs it is necessary to invoke differential stabilities of these mRNAs. The synchronous increase in the expression of both the steroidogenic enzymes and the mitochondrial oxidative phosphorylation system subunits, provides evidence for coregulation of steroidogenic and energy producing capacities of adrenal cells to meet the metabolic needs of steroid hormone production. Suppression of beta-actin gene expression may be related to changes in actin polymerization during ACTH-dependent cytoskeletal reorganization.

Adrenal Cortex↗