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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypothalamus-pituitary-adrenal (HPA) axis is stimulated during the course of certain immune, inflammatory and neoplastic processes. IL-1 is an important immunologically derived cytokine mediating the stimulation of this axis, although not the only one. We have compared the relative potencies of the cytokines IL-1, IL-6 and tumor necrosis factor (TNF), which share several biological actions, for stimulating ACTH and corticosterone output in freely-moving rats. Although all three cytokines can stimulate the HPA axis, IL-1 was the most potent. This effect of IL-1 was also present during the neonatal period, when the response of the HPA axis to acute stress is reduced in rodents. The results support the existence of an immune-HPA axis circuit. The biological and clinical relevance of this circuit is discussed.
J Steroid Biochem Mol Biol 1991
PMID:Cytokines as modulators of the hypothalamus-pituitary-adrenal axis. 165 87

The effect of immobilization stress on the expression of c-fos protein in the adrenal cortex of adult rats was investigated immunocytochemically. After immobilization stress lasting for longer than 30 min, an enhanced c-fos-like immunoreactivity was observed in the cortical cells of the zona fasciculata and zona reticulata. Compared to unstressed controls, an about 5-fold increase in the density of the immunoreactive cells in a unit of the cortical area was seen following a 1-h immobilization. The enhanced immunoreactivity lasted for at least 3 h after 1-h immobilization and it began to diminish 5 h after the stress. Furthermore, administration of dexamethasone 2 h prior to 1-h immobilization attenuated the stress-enhanced immunostaining for the c-fos-like protein. These results suggest that an acute stress may cause a dramatic and long-persisting induction of c-fos-like protein in the cortical cells of rat adrenals. The characteristic zonal distribution of the c-fos induction in rat adrenals as well as the effect of dexamethasone suggest involvement of the pituitary adrenocorticotropic hormone (ACTH) in the induction.
Mol Cell Endocrinol 1989 Oct
PMID:Induction of c-fos-like protein in the rat adrenal cortex by acute stress--immunocytochemical evidence. 255 26

It is apparent from the above discussion that acute stress, such as ischemia and reperfusion, hypoxia and reoxygenation, hyperthermia and oxidative stress, can rapidly potentiate the induction of genes for certain members of the HSP families and for antioxidants/antioxidant enzymes. Whether the stress response and induction of these genes have a direct role in myocardial protection is not known, but the induction of the expression of these genes are mostly associated with the preservation of myocardial cells from subsequent injury resulting from ischemia, hypoxia and reperfusion. The ubiquitous presence of some of these stress genes, such as for HSP 70 and catalase, in normal unstressed myocardium further suggests a role of these genes in many basic and essential biochemical and metabolic pathways. It is reasonable to speculate that the cells respond to the stress as a consequence of perturbations of one or more of the metabolic pathways by stimulating the induction of the stress genes of that particular pathway in which they participate. Thus, these genes are likely to be involved both in the protection and recovery/repair mechanisms. The precise mechanism by which myocardial cell recognizes and responds to a particular stress agent such as ischemia, hypoxia, hyperthermia or oxidative stress is not clear. While it is tempting to speculate that a generalized mechanism exists, applying to all different modes of stress response and gene induction, whether these agents induce the response via independent pathways or converge within a single point is entirely unclear. However, from the striking resemblance between the pattern of gene expression, especially with regard to HSP and antioxidant genes, it is reasonable to hypothesize the existence of a common and essential pathway of molecular signaling that leads to the expression of these stress genes (Fig. 2). The identification and characterization of the transcription factors that regulate the expression of the genes induced by these forms of stress should greatly facilitate our future understanding of the mechanism of stress response.
J Mol Cell Cardiol 1995 Jan
PMID:Gene expression in acute myocardial stress. Induction by hypoxia, ischemia, reperfusion, hyperthermia and oxidative stress. 776 Mar 41

The aim of this study was to examine by quantitative in situ hybridization the effects of an acute stress on the expression of the POMC gene in the mediobasal hypothalamus (MBH) of the rat. In control animals, the highest levels of POMC mRNA were observed in the posterior periventricular region of the MBH. Lower levels were found in the anterior and posterior arcuate nucleus. At the end of a one hour immobilization, a small decrease (-8%) was observed in the periventricular region only. Four hours after the end of immobilization, increases in POMC mRNA levels were detected in the anterior part (7%), in the posterior part (25%) and in the periventricular region (13%) of the MBH. These results suggest that MBH POMC-derived peptides might be an important component in the central response to stress.
Brain Res Mol Brain Res 1994 Oct
PMID:Effects of an acute immobilization stress upon proopiomelanocortin (POMC) mRNA levels in the mediobasal hypothalamus: a quantitative in situ hybridization study. 785 43

We investigated the acute effects of surgery, i.e. ovariectomy, the long-term effects of ovariectomy, and the effects of progesterone on the peripheral aromatization of androstenedione in rhesus monkeys (Macaca mulatta). For the acute effects of surgery, 7 rhesus monkeys were given a pulse of [3H]androstenedione/[14C]estrone 2 weeks before and immediately after ovariectomy. In each case all urine was collected for 4 days and analyzed for radioactivity as estrone glucuronide and the peripheral aromatization calculated from the isotope ratios. Similarly, 5 monkeys were studied before and 18 months after ovariectomy. The acute effects of surgery resulted in a significant decrease in the peripheral aromatization of androstenedione to estrone from a mean +/- SE of 0.94 +/- 0.26 to 0.61 +/- 0.19%, P = 0.0452. Conversely, the long-term effects of ovariectomy resulted in a significant increase in peripheral aromatization from 0.38 +/- 0.06 to 0.67 +/- 0.12%, P = 0.0207. In 7 monkeys the peripheral aromatization was measured before and 10 days after the administration of progesterone, 100 mg in oil. There was no difference in peripheral aromatization before, 0.62 +/- 0.04% and after progesterone, 0.58 +/- 0.05%, P = 0.10. We conclude that the acute stress of ovariectomy, or possibly the loss of ovarian aromatizing tissue, results in a decline in peripheral aromatization, but ovariectomy will have the long-term effect of an increase in aromatization, and that the presence or absence of progesterone does not play a role.
J Steroid Biochem Mol Biol 1994 Apr
PMID:The effects of ovariectomy and progesterone on peripheral aromatization in the female rhesus monkey. 818 Jan 18

In rats, acute immobilization (IMO) stress (2 h) induced a fall in the serum androgen concentrations (T+DHT) without detectable changes in serum luteinizing hormone (LH) values. In vitro studies, using a suspension of Leydig cells from adult rat testis, demonstrated that acute stress inhibited conversion of progesterone (P) or 17hydroxyprogesterone (17OHP) to T while conversion of androstendione (delta 4 A) was not affected. Acute IMO reduced activity of 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) and decreased basal and hCG-stimulated progesterone and androgen production. Chronic IMO stress (2 h daily for 10 days) induced a decrease in serum androgen level with decline in serum LH values. In vitro, hCG-stimulated progesterone and androgen production by suspension of Leydig cells, as well as conversion of P and 17OHP to T were not significantly altered. Our data demonstrates that acute IMO stress impaired testicular steroidogenesis primarily at the testicular level (decreasing the activity of certain enzymes), while chronic IMO stress exerts the effect mainly on the hypothalamic-pituitary axis; reduced serum LH levels elicit a decrease in serum androgen levels.
J Steroid Biochem Mol Biol 1996 Jun
PMID:Effects of acute and chronic immobilization stress on rat Leydig cell steroidogenesis. 883 69

To test the authors' hypothesis that cellular antioxidant enzymes constitute a cellular defense against acute stress, myocardial ischemia reperfusion injury in transgenic mice overexpressing the cellular glutathione peroxidase (GSHPx-1) was studied. Transgenic mice were generated using the entire mouse GSHPx-1 gene including approximately 2.0 kb 5'flanking sequence. A 400% increase of GSHPx activity was found in the hearts of transgenic mice compared with non-transgenic controls. Isolated perfused hearts were prepared from two groups of mice: transgenic overexpressed; non-transgenic controls. Hearts were perfused by Langendorff mode, and after 10 min of stabilization subjected to 30 min of ischemia followed by 20 min of reperfusion. In addition, a group of hearts were perfused for 50 min without subjecting them to ischemia and reperfusion to demonstrate the stability of heart preparation. Transgenic mouse hearts demonstrated significantly improved recovery of contractile force and the rate of contraction, compared to non-transgenic control mouse hearts. The infarct size was also lower in transgenic mouse hearts compared to those of non-transgenic controls. In concert, following ischemia, release of creatine kinase from the transgenic hearts was significantly lower than the control group. The results of this study indicate that increased GSHPx-1 expression renders the heart more resistant to myocardial ischemia reperfusion injury.
J Mol Cell Cardiol 1996 Aug
PMID:Transgenic mice overexpressing glutathione peroxidase are resistant to myocardial ischemia reperfusion injury. 887 85

Surfactant proteins A (SP-A) and D (SP-D) are "collectins": proteins with collagen-like region and lectin domain that bind carbohydrates in a calcium-dependent manner. Mannose-binding protein, a serum collectin, is an acute-phase protein. We hypothesized that SP-A and SP-D would respond to an acute stress, such as lung inflammation, in the same manner as does mannose-binding protein, with increased messenger ribonucleic acid (mRNA) and protein production. Rats received intratracheal lipopolysaccharide (LPS; 0.5 mg/kg) or vehicle and were killed 1, 6, 24, and 72 h later. Their lungs were lavaged and the lung tissue homogenized and analyzed for SP-A, SP-D, and phospholipids. Tissue levels of SP-A were increased by 6 h, peaked at 24 h, and were still elevated at 72 h in LPS-treated animals as compared with those given vehicle. SP-A and SP-D levels in lavage fluid were significantly elevated at 72 h. Message levels for SP-A and SP-D, but not SP-B, were significantly increased at 24 h. Lavage phospholipid levels first increased, then decreased in both the control and LPS-treated animals, and significantly less phospholipid was recovered in the lavage fluid of the LPS-treated animals than in that of controls at 72 h. Although other mechanisms, including altered surfactant metabolism, may be involved, these data are consistent with our hypothesis that SP-A and SP-D are upregulated by an acute inflammatory stress in a manner analogous to that of the structurally and functionally related serum acute-phase reactant, mannose-binding protein. We speculate that this upregulation may be a protective response for the lungs.
Am J Respir Cell Mol Biol 1996 Oct
PMID:Surfactant proteins A and D increase in response to intratracheal lipopolysaccharide. 887 85

Neuroendocrine-immune interactions are profoundly regulated by corticotropin-releasing hormone (CRH) indirectly, through activation of a global stress response, and directly, through pro-inflammatory actions on peripheral immune functions. The indirect effects of stress on immune/inflammatory responses occur via the stress-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic/adrenomedullary system. We have demonstrated that glucocorticoids and catecholamines favor T helper 2 (TH2) over T helper 1 (TH1) immune cells and mediators, by controlling the production of specific key regulatory cytokines. This could explain the influences of chronic stress on the development, course, and pathology of certain allergic, autoimmune/inflammatory, infectious, and neoplastic diseases. We have also shown that 'immune CRH' is secreted peripherally and plays a direct immunomodulatory role as an autocrine or paracrine mediator of inflammation. Upon release from immune cells and peripheral sensory afferent and/or postganglionic sympathetic nerves, CRH acts locally to elicit pro-inflammatory responses. This would explain the triggering or exacerbation of certain allergic or vasokinetic states by acute stress.
Mol Psychiatry 1997 Sep
PMID:The role of corticotropin-releasing hormone in neuroendocrine-immune interactions. 932 25

Corticosterone regulates a wide range of physiological parameters. Two receptors for corticosterone have been identified, the mineralocorticoid (type I) receptor (MR) and the glucocorticoid (type II) receptor (GR). To determine the relative role of these two receptors in mediating the effects of endogenous corticosterone, many studies have relied on the use of putative selective corticosteroid receptor antagonists. This study further examined the in vivo receptor selectivity of two compounds, RU28318 and RU40555 that are believed to be selective antagonists for MR and GR, respectively. Acute treatment of adrenalectomized rats with RU28318 (10-50 mg/kg) selectively decreased ex-vivo available MR binding in the hippocampus, whereas acute treatment with RU40555 (10-30 mg/kg) selectively decreased available GR binding in the hippocampus and pituitary. These receptor binding measures suggest that RU28318 in vivo selectively occupied MR, and that RU40555 in vivo selectively occupied GR. In functional studies, RU28318 (50 mg/kg) blocked the normalizing effect of aldosterone (120 microg/kg) on saline intake of adrenalectomized rats. RU40555 (30 mg/kg) blocked the suppressive effect of dexamethasone (50 microg/kg) on acute stress-induced corticosterone secretion. These studies further support the in vivo corticosteroid receptor selectivity of these two compounds and confirms their effective corticosteroid antagonistic properties.
J Steroid Biochem Mol Biol 1998 Nov
PMID:Evaluation of RU28318 and RU40555 as selective mineralocorticoid receptor and glucocorticoid receptor antagonists, respectively: receptor measures and functional studies. 987 80


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