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Interleukin 6 (IL-6) plays an important role in stress response and glucocorticoid action on the brain. It has been also shown that IL-6 plays a significant role in physiological and pathological brain development and is a crucial factor in the effects of prenatal immune challenge on physiological and behavioral abnormalities in adult offspring. We examined involvement of IL-6 in stressinduced changes in behavior and brain mechanisms in the adult mice. The PhenoRack system was used to non-invasively monitor mice home cage activity. Behavior of wild type mice C57BL/6J and IL-6 -/- knockout (IL-6 KO) mice were observed for 3 days using the PhenoRack system, which enables non-invasive monitoring of the mice home-cage activity (distance travelled, speeds and duration of movement, freezing). Mice were also subjected to standard behavioral tests. The open field test was used to establish the balance between exploratory behavior and anxiety evoked by the unknown, potentially dangerous situation. We measured the distance travelled in the open part of the arena, as well as time spent in it. We observed the sex-dependent effect of IL-6 on exploratory behavior. In all tested parameters IL-6 deficient females showed less anxiety than the wild type females. There was no difference in behavior in the open field between wild type and IL-6 deficient males. After finishing behavioral tests, the animals were killed with an overdose of pentobarbital and their brains were perfused transcardially with saline (0.9% NaCl) followed by 4% paraformaldehyde in 0.1 M phosphate buffer. The brains were cut on a cryostat into 40 µm sections and collected into 10 parallel series. Two of these series were stained with antibodies against glucocorticoid (GR) and mineralocorticoid (MR) receptors. One series from each brain was Nissl-stained for delineation of borders of the brain structures and evaluation of the number of cells in some of them. The number of hippocampal neurons and GRimmunopositive neurons in an area was estimated using the StereoInvestigator system (MicroBrightField Inc). Due to the crucial role of IL-6 in development of the hippocampus we evaluated the total number of cells in the CA1 field. We found that IL-6- deficient mice had significantly lower number of cells in the CA1 field and that almost all cells, unlike in wild-type mice, expressed the glucocorticoid receptor. Our preliminary results demonstrated that IL-6 is implicated in stress. Supported by the Polish National Science Center grant No 1577
 Glucocorticoid receptor (GR) is a steroid hormone receptor that has been shown to play important roles in diverse cellular and physiological processes. More and more evidence has revealed that the effects of glucocorticoids are mediated by the glucocorticoid receptor through genomic or nongenomic mechanisms. A growing number of glucocorticoid receptor splice variants have been identified in human tissues, but few are known in rat tissues. In this work, a novel rGR cDNA, called rGRβ, was cloned from Sprague Dawlay (SD) rat liver. Sequence analysis revealed that the rGRβ mRNA was 39 base pairs (bp) shorter than the rGR mRNA reported earlier. The deleted segment is located in exon 1 and encodes 13 repeated glutamine residues. Both the rGR and rGRβ mRNAs were quantitated by Northern blot hybridization using non-homologous glucocorticoid cDNA probes. Results showed that the rGR and rGRβ mRNAs were most abundant in the lung, the least abundant in the heart, and there were more rGR and rGRβ mRNAs in the kidney than in the liver. The identification of rGRβ may contribute to the understanding of the genomic or nongenomic effects of glucocorticoids.
Stress is considered to be a risk factor of several diseases. The following hypotheses were tested: (1) single exposure to an intensive stressor is followed by endothelial stimulation and/or damage to endothelial cells, (2) potential stress-induced endothelial cell damage is reduced by repeated pretreatment with pentoxifylline and (3) pentoxifylline treatment modifies neuroendocrine activation during stress reflected by changes in hypothalamic-pituitary-adrenocortical (HPA) axis function. Rats were treated with saline or pentoxifylline (20 mg/kg, s.c.) once daily for 7 days and then exposed to single immobilization stress for 20 or 120 min. In saline pretreated rats, stress exposure was followed by a rise in endothelaemia, von Willebrand factor concentrations, adrenocorticotropic hormone (ACTH) and corticosterone release, as well as by enhanced gene expression of hypothalamic corticotropin releasing factor (CRH). Stress-induced changes were reduced by pretreatment with pentoxifylline. Significant inhibition was observed in endothelaemia, plasma ACTH and corticosterone concentration in the adrenals. Thus, signs of endothelial injury as well as stress-induced hormone levels were reduced by pretreatment with pentoxifylline, although there is no evidence for a causal relationship. This protective action of pentoxifylline might be of benefit in the prevention and therapy of some stress-related disorders.
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The annexin-1 knockout mouse: what it tells us about the inflammatory response

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The 37kDa protein annexin 1 (Anx-1; lipocortin 1) is a glucocorticoid-regulated protein that has been implicated in the regulation of phagocytosis, cell signalling and proliferation, and postulated to be a mediator of glucocorticoids action in inflammation and in the control of anterior pituitary hormone release. Immuno-neutralisation or antisense strategies support this hypothesis as they can reverse the effect of glucocorticoids in several systems. We recently generated a line of mice lacking the Anx-1 gene noting that some tissues taken from such animals exhibited an increased expression of several proteins including COX-2 and cPLA2. In models of experimental inflammation, Anx-1-/- mice exhibit an exaggerated response and a partial or complete resistance to the anti-inflammatory effects of glucocorticoids. Several other anomalies were noted including abnormal leukocyte adhesion molecule expression, an increased spontaneous migratory behaviour of PMN in Anx-1-/- mice and a resistance in Anx-1-/- macrophages to glucocorticoid inhibition of superoxide generation. This paper reviews these and other data in the light of the development of the ‚second messenger™ hypothesis of glucocorticoid action.
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