Reciprocal influences between the signalling pathways regulating proliferation and steroidogenesis in adrenal glomerulosa cells

Foster, Richard H.

doi:10.1677/jme.0.0320893

Cited by 33 publications

(19 citation statements)

References 86 publications

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“…In addition, our results reveal a marked sexual dimorphism in the adrenal glands of CD1 mice, affecting not only the weight and size of the gland but also the secretion of corticosterone and aldosterone, steroid hormones that are regulated mainly by ACTH secretion and by the renin-angiotensin system and plasma potassium concentration, respectively (16,34,51). This sexdependent dimorphism in the murine adrenals, with corticosterone and aldosterone values higher in females than in males, is in agreement what that found in rats and humans (1,23,25,27,30,45,56).…”

Section: Discussionmentioning

confidence: 65%

Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Bastida¹,

Cremades²,

Castells³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Bastida CM, Cremades A, Castells MT, López-Contreras AJ, López-García C, Sánchez-Mas J, Peñ afiel R. Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels. Am J Physiol Endocrinol Metab 292: E1010 -E1017, 2007. First published December 5, 2006; doi:10.1152/ajpendo.00316.2006.-Adrenal sexual dimorphism is thought to be important in explaining sex-related differences regarding prevalent diseases and the responses to stress and drugs. We report here that in CD1 mice there is marked sexual dimorphism affecting not only gland size and corticoid hormone secretion but also adrenal ornithine decarboxylase (ODC), polyamine, and catecholamine levels in which testosterone appears to be a major determinant. Our results show that adrenal weight, ODC activity, and corticosterone and aldosterone secretion were higher in female than in male mice and that orchidectomy brought these male parameters closer to the values found in females. mRNA levels of steroidogenic proteins SF-1, Dax-1, steroid 21-hydroxylase, and aldosterone synthase appeared to be slightly higher in female than in male adrenals. Immunocytochemical analysis of adrenal ODC revealed that immunoreactivity was higher in females than in males and was located mainly in the cortical cells, and especially in zona glomerulosa, whereas no sex differences in ODC mRNA levels were observed. These results suggest that sex-associated differences in the expression of ODC in the mouse adrenal gland appear to be related mainly to posttranscriptional mechanisms. Combination treatment of mice with ␣-difluoromethylornithine (a suicide inhibitor of ODC) and a polyamine-deficient diet produced a marked decrease in adrenal polyamine and catecholamine levels and a significant reduction in plasma corticosterone and aldosterone concentrations that were not associated with a decrease in the mRNA levels of steroidogenic proteins. All of these data suggest a relevant role for testosterone, ODC, and polyamines in the mouse adrenal function. mice; ␣-difluoromethylornithine; corticosterone; aldosterone; steroidogenesis THE ADRENAL GLAND plays an important role in stress response, with the hypothalamic-pituitary-adrenal axis and the sympatho-adrenomedulary system as the principal components (41). Considerable evidence has accumulated indicating that gonadal factors act as regulators of the hypothalamic-pituitary-adrenal axis and adrenal function. In the rat there is a marked sexual dimorphism in adrenal weight, plasma ACTH, and corticosterone concentrations, with females having higher values than males (1,25,27,30,45). This adrenal sexual dimorphism is thought to be an important factor in explaining sex differences in relation to prevalent diseases associated with hypothalamic-pituitary-adrenal axis reactivity, such as cardiovascular disease, inflammation, diabetes, and hypertension (19,55). On the other hand, it has been suggested that a transient increase in ornithine decarboxylase (ODC) activity and tissue p...

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Section: Discussionmentioning

confidence: 65%

Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Bastida¹,

Cremades²,

Castells³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Bovine adrenal cells, which express several GPCRs (including those for LPA, Ang II, bradykinin, and ET-1), as well as RTKs for EGF and FGF (9,43), provide a physiological model for investigation of the mechanism(s) of cross-communication between these receptors during ERK1/2 activation. One of the major mechanisms mediating crosscommunication between GPCRs and RTKs is the activation of MMPs that cause release of several ligands such as heparin binding-EGF (HB-EGF), amphiregulins, transforming growth factor-α (TGF-α), fibroblast growth factor (FGF) and tumor necrosis factor-α (TNF-α), which bind to and activate the EGF-R (26,32,35,38).…”

Section: Discussionmentioning

confidence: 99%

“…However, little information is available on the signaling pathways involved in the activation of mitogen-activated protein kinases (MAPKs) by GPCRs and RTKs in adrenal glomerulosa cells. Moreover, the extent to which cross-communication between GPCRs and RTKs occurs in these cells has not been established (9).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of endothelin-1-induced MAP kinase activation in adrenal glomerulosa cells

Shah

Báukal

Chen

et al. 2006

The Journal of Steroid Biochemistry and Molecular Biology

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G protein-coupled receptors (GPCRs) such as angiotensin II, bradykinin and endothelin-1 (ET-1) are critically involved in the regulation of adrenal function, including aldosterone production from zona glomerulosa cells. Whereas substantial data are available on the signaling mechanisms of ET-1 in cardiovascular tissues, such information in adrenal glomerulosa cells is lacking. Bovine adrenal glomerulosa (BAG) cells express receptors for endothelin-1 (ET-1) and their stimulation caused phosphorylation of Src (at Tyr416), proline-rich tyrosine kinase (Pyk2 at Tyr402), extracellularly regulated signal kinases (ERK1/2), and their dependent proteins, p90 ribosomal S6 kinase (RSK-1) and CREB. ET-1 elicited these responses predominantly through activation of a G i -linked cascade with a minor contribution from the G q /PKC pathway. Whereas selective inhibition of EGF-R kinase with AG1478 caused complete inhibition of EGF-induced ERK/ RSK-1/CREB activation, it caused only partial reduction (30-40%) of such ET-1-induced responses. Consistent with this, inhibition of matrix metalloproteinases (MMPs) with GM6001 reduced ERK1/2 activation by ET-1, consistent with partial involvement of the MMP-dependent EGF-R activation in this cascade. Activation of ERK/RSK-1/CREB by both ET-1 and EGF was abolished by inhibition of Src, indicating its central role in ET-1 signaling in BAG cells. Moreover, the signaling characteristics of ET-1 in cultured BAG cells closely resembled those observed in clonal adrenocortical H295R cells. The ET-1-induced proliferation of BAG and H295 R cells was much smaller than that induced by Ang II or FGF. These data demonstrate that ET-1 causes ERK/RSK-1/CREB phosphorylation predominantly through activation of G i and Src, with a minor contribution from MMP-dependent EGF-R transactivation.

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“…Steroid hormones like testosterone, progesterone, cortisol, aldosterone, and estradiol are important endocrine chemical messengers that are involved in a vast number of physiological processes including metabolism, inflammation, electrolyte and fluid balance, and secondary sex differentiation (Foster, 2004;Ghayee and Auchus, 2007;Newton and Holden, 2007;Williams-Ashman and Reddi, 1971). Steroid hormone synthesis occurs in the gonads, adrenal gland, placenta, intestines (Abdallah et al, 2004;Ghayee and Auchus, 2007;Mueller et al, 2007;Payne and Hales, 2004), and has recently been characterized in brain and peripheral nervous system tissues Mellon, 2007;Tsutsui et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Multiple Roles for Sphingolipids in Steroid Hormone Biosynthesis

Lucki

Sewer

Subcellular Biochemistry

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Steroid hormones are essential regulators of a vast number of physiological processes. The biosynthesis of these chemical messengers occurs in specialized steroidogenic tissues via a multistep process that is catalyzed by members of the cytochrome P450 superfamily of monooxygenases and hydroxysteroid dehydrogenases. Though numerous signaling mediators, including cytokines and growth factors control steroidogenesis, trophic peptide hormones are the primary regulators of steroid hormone production. These peptide hormones activate a cAMP/ cAMP-dependent kinase (PKA) signaling pathway, however, studies have shown that crosstalk between multiple signal transduction pathways and signaling molecules modulates optimal steroidogenic capacity. Sphingolipids such as ceramide, sphingosine, sphingosine-1-phosphate, sphingomyelin, and gangliosides have been shown to control the steroid hormone biosynthetic pathway at multiple levels, including regulating steroidogenic gene expression and activity as well as acting as second messengers in signaling cascades. In this review, we provide an overview of recent studies that have investigated the role of sphingolipids in adrenal, gonadal, and neural steroidogenesis.

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Reciprocal influences between the signalling pathways regulating proliferation and steroidogenesis in adrenal glomerulosa cells

Cited by 33 publications

References 86 publications

Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Mechanisms of endothelin-1-induced MAP kinase activation in adrenal glomerulosa cells

Multiple Roles for Sphingolipids in Steroid Hormone Biosynthesis

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