Corticotropin-releasing factor (CRF)-like immunoreactivity in the adrenal medulla

Hashimoto, Kozo; Murakami, Kazuharu; Hattori, Teruhiko; Niimi, Michio; Fujino, Kazuyuki; Ota, Zensuke

doi:10.1016/0196-9781(84)90011-1

Cited by 77 publications

(41 citation statements)

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“…First, the range of CRH concentrations found to be effective on apoptosis was similar to the range believed to be present within the adrenal medulla (32)(33)(34)(35)(36). Second, normal chromaffin cells, like the PC12 cells, have specific CRH binding sites (37,38).…”

Section: Crh Induces Fas Ligand Production-serum Deprivation Induced mentioning

confidence: 92%

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Dermitzaki

Tsatsanis

Gravanis

et al. 2002

Journal of Biological Chemistry

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Recent experimental findings involve corticotropinreleasing hormone (CRH) in the cellular response to noxious stimuli and possibly apoptosis. The aim of the present work was to examine the effect of CRH on apoptosis and the Fas/Fas ligand system in an in vitro model, the PC12 rat pheochromocytoma cell line, which is widely used in the study of apoptosis and at the same time expresses the CRH/CRH receptor system. We have found the following. CRH induced Fas ligand production and apoptosis. These effects were mediated by the CRH type 1 receptor because its antagonist antalarmin blocked CRHinduced apoptosis and Fas ligand expression. CRH activated p38 mitogen-activated protein kinase, which was found to be essential for CRH-induced apoptosis and Fas ligand production. CRH also promoted a rapid and transient activation of ERK1/2, which, however, was not necessary for either CRH-induced apoptosis or Fas ligand production. Thus, CRH promotes PC12 apoptosis via the CRH type 1 receptor, which induces Fas ligand production via activation of p38.Several lines of evidence suggest that corticotropin-releasing hormone (CRH) 1 may play a role in the cellular response to noxious stimuli that promote neuron death (1). Indeed, CRH contributes to hippocampal ischemic injury, an effect prevented by the CRH antagonist ␣-helical CRH (ahCRH) (2). Similarly, astressin, a potent CRH antagonist, exerts a considerable neuroprotective effect on hippocampal cell damage following kainic acid-induced excitotoxic seizures (3). In animal models of induced status epilepticus, CRH causes neuronal loss in limbic structures, including the CA3 region of the hippocampus characterized by pyramidal cell apoptosis (4). Furthermore, administration of CRH to the brain of immature rats is associated with progressive hippocampal CA3 neuron apoptosis independent of glucocorticoids (5). These phenomena involve cell apoptosis. However, there is no information regarding the effects of CRH on the apoptotic machinery.The Fas/Fas ligand system controls apoptosis of several types of immune cells and possibly of epithelial and neural cells including cells in hippocampus and cortex (6, 7). The aim of the present work was to examine the effect of CRH on apoptosis and Fas ligand expression in a well established in vitro model, the PC12 rat pheochromocytoma cell line, which has characteristics of epithelial and neuronal cells and is widely used as a model in the study of apoptosis. PC12 cells express the CRH/ CRH receptor and the Fas/Fas ligand systems, providing a physiological model for the study of the effects of CRH on apoptosis and the intracellular signaling cascade involved (8, 9). When PC12 cells that are differentiated by nerve growth factor (NGF) are deprived of growth factors, they undergo apoptosis via expression of Fas ligand (10). Expression of Fas ligand and apoptosis in differentiated PC12 cells and primary cultures of rat sympathetic neurons depends on activation of stress-activated protein (SAP) kinase, p38 mitogen-activated protein kinase (MAPK), a...

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Section: Crh Induces Fas Ligand Production-serum Deprivation Induced mentioning

confidence: 92%

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Dermitzaki

Tsatsanis

Gravanis

et al. 2002

Journal of Biological Chemistry

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“…VIP is not, however, the only adrenal peptide that could fulfil this role in theory. The gland has also been reported to contain corticotrophin releasing factor-like immunoreactivity (CRF) (Suda, Tomori, Tozawa, Mouri, Demura & Shizume, 1984;Hashimoto, Murakami, Hattori, Niimi, Fujino & Ota, 1984). Moreover, Gann and his co-workers have demonstrated recently that CRF is released in relatively substantial quantities from the adrenal in response to haemorrhage in conscious dogs (Bruhn, Engeland, Anthony, Gann & Jackson, 1987).…”

Section: Introductionmentioning

confidence: 99%

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Edwards¹,

Jones²

1988

The Journal of Physiology

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SUMMARY1. The output of corticotrophin releasing factor-like immunoreactivity (CRF) from the adrenal gland has been investigated using the 'adrenal clamp' technique in conscious calves.2. Stimulation of the peripheral end of the splanchnic nerve for 10 min increased the mean output of CRF progressively, so that it had risen by about twentyfold, to a peak incremental value of 24 +4 pmol min-' kg-' at 10 min. This response was significantly increased by stimulating in bursts at 40 Hz for 1 s at 10 s intervals, which raised the mean CRF output by 44+7 pmol min-' kg-' at 10 min (P < 0-05).3. The mean output of adrenaline and noradrenaline rose more abruptly in response to splanchnic nerve stimulation with peak incremental values realized within 2-5 min. However, the ratios of adrenal CRF to catecholamine output were closely similar during the later stages of stimulation (7-5-10 min). There was a similarly abrupt rise in adrenal cortisol output in response to splanchnic nerve stimulation which was, nevertheless, linearly related to arterial plasma ACTH concentration throughout.4. In hypophysectomized calves, administration of adrenocorticotrophic hormone (ACTH1-24) at a dose of 5 ng min-' kg-1 reduced the output of adrenal CRF in response to splanchnic nerve stimulation by about 50% (P < 0 05). 5. CRF isolated from adrenal venous effluent plasma, collected both at rest and during splanchnic nerve stimulation, was separated by reverse-phase high-pressure liquid chromatography and found to elute in a position identical to that of human 41CRF. This suggests that adrenal CRF is structurally closely similar to its pituitary counterpart.

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“…The adrenal medulla in particular produces and contains many neurotransmitters and peptide hormones other than CRF, such as neuropeptide Y, serotonin (5-HT), and vasoactive intestinal peptide; the presence has been established, but the functions are incompletely understood (Nussdorfer 1996, Ehrhart-Bornstein et al 1998. CRF is found exclusively in a subpopulation of medullary chromaffin cells (Hashimoto et al 1984, Suda et al 1984, Bruhn et al 1987a,b, Minamino et al 1988. Moreover, direct effects of CRF, independent of HPA-axis activation, have been demonstrated on adrenocortical steroid release (Bornstein et al 1990, Jones & Edwards 1992, van Oers et al 1992, Nussdorfer 1996.…”

Section: Introductionmentioning

confidence: 99%

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

Huising

Metz

et al. 2007

Journal of Endocrinology

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Corticotropin-releasing factor (CRF) plays a central role in the regulation of the stress axis. In mammals, CRF as well as its receptors and its CRF-binding protein (CRF-BP) are expressed in a variety of organs and tissues outside the central nervous system. One of these extrahypothalamic sites is the adrenal gland, where the paracrine actions of adrenal CRF influence cortical steroidogenesis and adrenal blood flow. Although the central role of CRF signaling in the initiation and regulation of the stress response has now been established throughout vertebrates, information about the possible peripheral presence of CRF in earlier vertebrate lineages is scant. We established the expression of CRF, CRF-BP, and the CRF receptor 1 in a panel of peripheral organs of common carp (Cyprinus carpio). Out of all the peripheral organs tested, CRF and CRF-BP are most abundantly expressed in the carp head kidney, the fish equivalent of the mammalian adrenal gland. This expression localizes to chromaffin cells. Furthermore, detectable quantities of CRF are released from the intact head kidney following in vitro stimulation with 8-bromo-cAMP in a superfusion setup. The presence of CRF and CRF-BP within the chromaffin compartment of the head kidney suggests that a pathway homologous to the mammalian intraadrenal CRF system is present in the head kidney of fish. It follows that such a system to locally fine-tune the outcome of the centrally initiated stress response has been an integral part of the vertebrate endocrine system since the common ancestor of teleostean fishes and mammals.

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Corticotropin-releasing factor (CRF)-like immunoreactivity in the adrenal medulla

Cited by 77 publications

References 14 publications

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Corticotropin-releasing Hormone Induces Fas Ligand Production and Apoptosis in PC12 Cells via Activation of p38 Mitogen-activated Protein Kinase

Secretion of corticotrophin releasing factor from the adrenal during splanchnic nerve stimulation in conscious calves.

Corticotropin-releasing factor (CRF) and CRF-binding protein expression in and release from the head kidney of common carp: evolutionary conservation of the adrenal CRF system

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