Ultrastructure of the Mammalian Adrenal Cortex

Idelman, S

doi:10.1016/s0074-7696(08)61248-6

Cited by 182 publications

(58 citation statements)

References 154 publications

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“…1). The fine structures of these cells corresponded to those reported previously (ZELANDER, 1957(ZELANDER, , 1959MOLBERT and ARNESEN, 1960;SATO, 1967;SHARDEIN et al, 1967;IDELMAN, 1970), except for the increase of lipofuscin and ceroid pigments and the appearance of occasional bizarre mitochondria (unpublished data).…”

Section: Resultssupporting

confidence: 88%

Specific Lamellar Structures of Agranular Endoplasmic Reticulum in the Senile Mouse Adrenal Cortex

Setoguti

Satou

Goto

1979

Arch. Histol. Jap., Arch. Histol. Jpn

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Section: Resultssupporting

confidence: 88%

Specific Lamellar Structures of Agranular Endoplasmic Reticulum in the Senile Mouse Adrenal Cortex

Setoguti

Satou

Goto

1979

Arch. Histol. Jap., Arch. Histol. Jpn

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“…We show that steroid treatment of mice downregulated VEGF-R2 (Flk-1/KDR) and that its expression was restored to control level by ACTH injections during 6 days. Such in vivo data indicate an overlapping with the timing of ACTH-induced proliferation of the adrenocortical zone observed in previous histomorphological studies (21). We also demonstrate that Flt-1 expression remained constant after steroid or ACTH treatment.…”

Section: Discussionsupporting

confidence: 89%

Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

Mallet

Féraud²,

Ouengue-Mbélé

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Mallet, Christine, Olivier Fé raud, Gaehl OuengueMbé lé , Isabelle Gaillard, Nicolas Sappay, Daniel Vittet, and Isabelle Vilgrain. Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH. Am J Physiol Endocrinol Metab 284: E156-E167, 2003; 10.1152/ajpendo.00450.2001.-Although ACTH is important to adrenal growth and steroidogenesis, its role in vascular development and function has not been established in vivo. In the present study, we demonstrate the expression of mRNA for all four VEGF isoforms (mVEGF120, 144, 164, 188) and for Flk-1/KDR and Flt-1 receptors in the mouse adrenal in vivo. Suppression of the pituitary adrenocortical axis by dexamethasone (0.5 mg ⅐ 100 g body wt Ϫ1 ⅐ day Ϫ1 during 6 days) induced a decrease in corticosterone levels, adrenal weights by 50% (P Ͻ 0.001), VEGF188 mRNA, and Flk-1/KDR mRNA, whereas Flt-1 remained consistent during steroid treatment. A daily injection of ACTH-(1-39) restored the transcript for Flk-1/KDR and both VEGF188 and plasma corticosterone to control levels. To gain further insights into the effects of ACTH, cultured endothelial cells (ECs) were treated with forskolin, which increases cAMP, the second messenger in ACTH action. We demonstrate that Flk-1/KDR protein expression was markedly increased by forskolin within 24-48 h of treatment in a dose-dependent manner (0.1-10 M). The biological effect of ACTH on ECs was then tested by use of coincubations of fasciculata cells and ECs in 3D-collagen assay. Within 5-7 days of culture, ECs organized into multicellular structures that resemble networks of microvasculature, which characterize angiogenesis in vitro. vascular endothelial growth factor receptors; adrenocorticotropin; angiogenesis; mouse adrenal; steroidogenesis; hypothalamo-pituitary disconnection; vascular permeability THE ADRENAL CORTEX is physiologically important as the site of formation and secretion of several steroid hormones and less-active steroids. The secreted hormones gain access to the bloodstream through an intense and complex adrenal vasculature that is essential for organ growth and maintenance. The vessels of the adrenal cortex are characterized by richly fenestrated endothelia (2, 40). These fenestrations are the pores through which releasing factors within the hemal milieu can access the cells. In adult mammals, adrenal growth and steroidogenesis are regulated by adrenocorticotropin (ACTH) (27), which acts through interaction with a specific melanocortin receptor (MC2R) specifically expressed in the adrenal cortex (6, 32). This guanine nucleotide-binding protein-coupled receptor elicits the activation of adenylate cyclase and the production of cAMP, which activate the protein kinase A-signaling pathway (39, 53) and the normal functioning of adrenocortical cells. Glucocorticoid hormones are thought to exert negative feedback inhibition on hypothalamic-pituitary-adrenocortical axis activity at the pituitary, hypothalamic, and extrahypothalamic levels. This ultimately results in decreased...

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“…1) and ACTH-treated (Fig. 4) rats in this study are in accordance with previous findings (25)(26)(27). These include, most noticeably, an increase in the number of mitochondria, lipid droplets, and smooth endoplasmic reticulum.…”

Section: Ultrastructuresupporting

confidence: 93%

Ultrastructure, Steroidogenic Potential, and Energy Metabolism of the Snell Adrenocortical Carcinoma 494

Kimmel¹,

Péron²,

Haksar³

et al. 1974

The Journal of Cell Biology

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Electron microscope studies were carried out with the adrenocortical carcinoma 494 and normal adrenal cortex tissue. The mitochondria of the tumor cells showed marked differences when compared with mitochondria from fasciculata cells of the normal adrenal cortex. These differences were primarily related to mitochondrial number and crista structure.Corticosterone production in isolated tumor cells was extremely low and neither ACTH nor dibutyryl cyclic AMP had any stimulatory effect. Normal adrenal cells showed at least a tenfold increase under identical conditions. In the presence of corticosteroid precursors the amount of corticosterone produced by the tumor cells was much less than that produced by normal cells.The results indicate a reduced capacity,for l l~-hydroxylation in the tumor mitochondria and a possible reduced capacity for biosynthetic steps before the 1 l~-hydroxylation reaction. Glycolysis in isolated tumor cells was also lower than in normal cells.Isolated tumor mitochondria oxidized succinate normally with a good degree of coupling with phosphorylation. However, unlike normal adrenal mitochondria, the tumor mitochondria showed little or no oxygen uptake with other Krebs cycle substrates. These data suggest that the tumor mitochondria may be lacking in the flavoprotein dehydrogenases responsible for the oxidation of NADH and NADPH, although other components of the respiratory chain may be intact.

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Ultrastructure of the Mammalian Adrenal Cortex

Cited by 182 publications

References 154 publications

Specific Lamellar Structures of Agranular Endoplasmic Reticulum in the Senile Mouse Adrenal Cortex

Specific Lamellar Structures of Agranular Endoplasmic Reticulum in the Senile Mouse Adrenal Cortex

Differential expression of VEGF receptors in adrenal atrophy induced by dexamethasone: a protective role of ACTH

Ultrastructure, Steroidogenic Potential, and Energy Metabolism of the Snell Adrenocortical Carcinoma 494

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