Age-related changes in the inner zone of the adrenal cortex of the rat—a morphologic and biochemical study

Almeida, Henrique; Magalhäes, Maria C.; Magalhães, M. M.

doi:10.1016/s0047-6374(98)00099-2

Cited by 24 publications

(26 citation statements)

References 46 publications

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“…with ACTH 2 IU/ 100 g b.w. as reported in previously published papers (Almeida et al 1998, Neves et al 2000 and killed 30 min, 2, 18 and 24 h after ACTH administration. In addition, two other groups were injected daily with ACTH 2 IU/100 g b.w.…”

Section: Time-course Studysupporting

confidence: 53%

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Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment

Ferreira¹,

Cruz²,

Neves³

et al. 2007

Journal of Endocrinology

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ACTH released from the pituitary acts through activation of cAMP/PKA in adrenocortical cells stimulating steroidogenesis. Although ACTH was originally thought to have antiproliferative effects on the adrenal, recently it has been described that it could also have proliferative effects acting through other signalling cascades. This is also relevant in humans given the increased levels of ACTH occurring together with adrenal cortex hyperplasia observed in Cushing's disease and possibly in other situations such as chronic stress. One of the signalling pathways regulating cell proliferation is the extracellular signal regulated kinase (ERKs) pathway. ERKs are members of the MAPK family of cascades. They are activated by extracellular stimuli such as growth factors and mitogens, become phosphorylated through MEK1/2 and regulate a diversity of cellular processes such as proliferation and differentiation. Until now, no study addressed the effects of chronic ACTH administration on the activation of ERKs in vivo. Using rats submitted to different ACTH dosages as well as variable durations, we determined if ACTH induced ERKs activation and by establishing a parallelism with proliferating cell nuclear antigen (PCNA) expression, we aimed to demonstrate a role of ACTH-induced ERKs activation in cell proliferation. Blood was collected for hormonal analysis and the role of ACTH-induced ERKs activation in the stimulation of steroidogenesis was also studied. We confirmed that ACTH increased adrenal weight and corticosterone levels when compared with control or dexamethasone-treated animals. We also demonstrated that ACTH increases ERKs activation and PCNA expression in a time-and dosedependent manner. When ERKs activation was blocked by the use of a specific MEK inhibitor (PD98059), there was a decrease in ACTH-induced corticosterone release and PCNA expression. We conclude that chronic ACTH induces ERKs activation and that this plays an important role in the induction of cell proliferation as well as steroidogenesis.

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Section: Time-course Studysupporting

confidence: 53%

“…with Synacthen Depôt (ACTH) in doses similar to those used in previously published papers (Pudney et al 1984, Watanabe et al 1997, Almeida et al 1998, Neves et al 2000, Thomas et al 2004, as well as with higher doses.…”

Section: Dose-response Studymentioning

confidence: 96%

Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment

Ferreira¹,

Cruz²,

Neves³

et al. 2007

Journal of Endocrinology

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“…Moreover, serum levels may not reflect brain neurosteroid concentrations (Corpechot et al, 1997). The influence of the adrenal gland may be important to consider, given that the adrenal gland produces neuroactive steroids that can increase excitability, such as corticosterone (albeit not at all concentrations), and corticosterone production appears to increase throughout adult life of the female rat (de Almeida et al, 1998;Sencar-Cupovic and Milkovic, 1976).…”

Section: Incidence Of Status Is Influenced By Agementioning

confidence: 99%

Seizure susceptibility in intact and ovariectomized female rats treated with the convulsant pilocarpine

Scharfman

Goodman

Rigoulot

et al. 2005

Experimental Neurology

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Despite numerous neuroendocrinological studies of seizures, the influence of estrogen and progesterone on seizures and epilepsy remains unclear. This may be due to the fact that previous studies have not systematically compared distinct endocrine conditions and included all relevant controls. The goal of the present study was to conduct such a study using pilocarpine as chemoconvulsant. Thus, age and weight-matched, intact or ovariectomized rats were tested to determine incidence of status epilepticus and to study events leading to status. Intact female rats were sampled at each cycle stage (proestrus, estrus, metestrus, or diestrus 2). Convulsant was administered at the same time of day, 10:00-10:30 a.m. Statistical analysis showed that there was a significantly lower incidence of status on the morning of estrus, but differences were attenuated in older animals. Ovariectomized rats were distinct in their rapid progression to status. These results show that the incidence of status in female rats following pilocarpine injection, and the progression to pilocarpineinduced status, are influenced by reproductive state as well as age. The hormonal milieu present specifically on the morning of estrus appears to decrease susceptibility to pilocarpine-induced status, particularly at young ages. In contrast, the chronic absence of reproductive steroids that characterizes the ovariectomized rat leads to a more rapid progression to status. This dissociation between incidence vs. progression provides new insight into the influence of estrogen and progesterone on seizures.

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“…Despite the fact that GH exerts an evident growthstimulating effect on adrenal cortex (for review see ref. 25), aging is normally associated with a rise in the weight and volume of adrenals, at least in the rat (26,27). This may be due to the aging-dependent impairment of adrenocortical secretion, which, by releasing hypothalamo-pituitary corticotrope complex from glucocorticoid negative feed-back, causes an increase in the level of circulating ACTH (for review see refs.…”

Section: Discussionmentioning

confidence: 99%

Age-dependent decrease in the ghrelin gene expression in the human adrenal cortex: A real-time PCR study

Carraro

Albertin²,

Aragona³

et al. 2006

Int J Mol Med

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Abstract. Numerous lines of evidence indicate that ghrelin, an endogenous ligand of the growth hormone-secretagogue receptor, is expressed in the human and rat adrenal cortex. In this study, we examined whether ghrelin gene expression undergoes changes in the human adrenal cortex during aging. Semi-quantitative real-time reverse transcription-polymerase chain reaction demonstrated a highly significant negative correlation between ghrelin mRNA and age in adrenal cortexes of 27 patients (aged from 33 to 82 years), who underwent unilateral adrenalectomy/nephrectomy for kidney cancer. No significant differences in the level of adrenal ghrelin expression were observed between males and females. Since it has been previously shown that ghrelin exerts a marked growthstimulating action on cultured adrenocortical cells, we hypothesize that the down-regulation of ghrelin gene transcription in adrenals could be associated with the reported decrease in adrenal DNA synthesis and mitogenic activity during aging.

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Age-related changes in the inner zone of the adrenal cortex of the rat—a morphologic and biochemical study

Cited by 24 publications

References 46 publications

Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment

Increased extracellular signal regulated kinases phosphorylation in the adrenal gland in response to chronic ACTH treatment

Seizure susceptibility in intact and ovariectomized female rats treated with the convulsant pilocarpine

Age-dependent decrease in the ghrelin gene expression in the human adrenal cortex: A real-time PCR study

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