• The Korean Journal of Zoology
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• v.38 no.3
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• pp.426-432
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• 1995

Expression of $\beta$-lactoglobulin gene in mammary tissue is strongly induced by lactogenic hormones such as prolactin, glucocorticoid, and insulin. In order to elucidate the regulatory mechanism underlying such hormonal induction, the response of the caprine $\beta$-lactoglobulin gene promoter to lactogenic hormones was analyzed in cultured HC11 mammary cells. Expression with serial deletions of the 5' -regulatory sequence of the $\beta$-lactoglobulin promoter revealed that two regions are responsible for a substantial change in hormonal indudbility. The region upstream of-1692, which exhibited strong repression of the downstream promoter, mediated the induction by insulin. This insulin-response was independent of the other two lactogenic hormones, prolactin and glucocorticoid. The other region from -740 to -470, which showed strong activation of the $\beta$-lactoglobulin promoter in confluent HC11 mammary cells, mediated mainly the response to a glucocorticoid analogue, dexametasone. The induction by the latter region, however, was suppressed by the usptream repression without insulin treatment. These results suggest that the induction of $\beta$-lactoglobulin promoter activity by lactogenic hormones in mammary cells may be achieved by the combined action of derepression by in sulin and activation by glucocorticoid and prolactin. Dexametasone response by the latter region seems to be mediated by the glucocorticoid receptor site around -7OObp.

• Journal of Marine Bioscience and Biotechnology
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• v.2 no.2
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• pp.81-85
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• 2007

Glucocorticoid hormone regulates numerous physiological processes, such as regulation of metabolism, and anti-inflammatory and immunosuppressive actions via the activation and repression of gene expression. Here we described a lentivirus-based reporter vector system expressing red fluorescent protein (mRFP) or firefly luciferase (Luc) under the control of a glucocorticoid-responsive element that allows observation of the temporospatial pattern of glucocorticoid induced GR-mediated signaling on a cellular level. Moreover, usage of the chromatin insulator of the chicken ${\beta}$-globin locus induced a marked increase of sensitivity of glucocorticoid inducible promoter of a reporter gene. Use of this method will be applicable of screening for agonist and antagonist of GR in vitro, and also a reporter gene assay for the in vivo determination of the GR-mediated gene activation.

• Journal of Life Science
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• v.17 no.3 s.83
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• pp.305-311
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• 2007

Glucocorticoids (GCs) alter metabolism, synaptogenesis, apoptosis, neurogenesis, and dendritic morphology in the hippocampus. To better understand how glucocorticoids regulate these aspects of hippocampal biology, we studied gene expression patterns in the CA3 (Hippocampal pyramidal cell field CA3) and dentate gyrus (DG). Litter-matched Lewis inbred rats treated for 20 days with either 9.5 mg per day sustained-release corticosterone or placebo pellets were compared with high-density oligonucleotide microarray analysis (Rat Neurobiology U34 Arrays, Affymetrix). In placebo-treated rats, 32 genes were expressed at greater levels in CA3 than DG, whereas 3 genes were expressed at great levels in DC than CA3. Regional differences were also apparent in corticosterone-induced changes in the hippocampal transcriptome. Six genes in CA3 and 41 genes in DC were differentially regulated by corticosterone. As per the glucocorticoid effects on gene transcription in the brain, forty three of these genes were upregulated, and 4 genes were downregulated. Genes differentially expressed in hippocampus included those for 13 neurotransmitter proteins, 5 ion channel related proteins, 4 transcription factors, 3 neurotrophic factors, 1 cytokine, 1 apoptosis related protein, and 5 genes involved in synaptogenesis. Interestingly, GCs can have suppressive effects on brain BDNF mRNA transcription, one of the neurotrophic factors. These results indicate the diversity of targets affected by chronic exposure to corticosterone and highlight important regional differences in hippocampal neurobiology.

• Women's Health Nursing
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• v.21 no.2
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• pp.106-114
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• 2015

Purpose: The purpose of this review was to describe a psychoneuroimmunology (PNI) framework for postpartum depression (PPD) and discuss its implications for nursing research and practice for postpartum women. Methods: This study explored the role of hypothalamic-pituitary-adrenal (HPA) axis and inflammation as possible mediators of risk factors for PPD through literature review. Results: From this PNI view, human bodies are designed to respond with the reciprocal interactions among the neuro-endocrine and immune system when they are faced with physical or psychological stressors. Chronic stress induces alterations in the function of HPA axis, and a chronic low-grade inflammatory response is associated with depression. The dysfunctions of cytokines and HPA axis have been observed during the postpartum period. Stress promotes glucocorticoid receptor resistance, which can promote inflammatory responses. This, in turn, can contribute to the pathophysiology of depression. This can especially affect populations at vulnerable time-points, such as women in the postpartum. Conclusion: From a PNI perspective, well-designed prospective research evaluating the role of stress and inflammation as an etiology of PPD and the effect of stress reduction is warranted to prevent PPD.

• Journal of Korean Biological Nursing Science
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• v.18 no.1
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• pp.36-42
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• 2016

Purpose: Stress activates the sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) axis and induces the release of glucocorticoids. Saccharin is 300 times sweeter than sucrose, but does not increase blood insulin levels. Thus, this study was designed to evaluate the effect of saccharin intake in restraint-induced stress response reduction in rats. Methods: Adult male Sprague-Dawley (SD) rats had stress induced by restraint for 2 hours/day for 1 week. Saccharin was provided in sufficient amounts to allow them to intake it voluntarily at 0.1% diluted in water. The Y-maze test and forced swim test (FST) were performed to evaluate cognitive function and the depressive behavior of the rats. The protein expression of the glucocorticoid receptor (GR) in hippocampal cornu ammonis (CA) 1 was investigated by using immunohistochemistry. Results: It was found that, the percentage of alternation in the Y-maze test was significantly (p<.01) higher in the Stress + saccharin group than in the Stress group. Immobility time in the FST was significantly (p<.01) lower in the Stress + saccharin group than in the Stress group. Also, the positive cells of GR in hippocampus CA1 were significantly (p<.05) lower in the Stress + saccharin group than in the Stress group. Conclusion: This study showed that there was an effect of saccharin intake in restraint-induced stress response reduction in rats.

• Development and Reproduction
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• v.4 no.2
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• pp.221-229
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• 2000

Lactogenesis in mammary gland is under the control of various lactogenic hormones including hypophysial growth hormone and prolactin. Recent studies reported that such pituitary lactogenic hormones are also expressed in mammary cells as well as in pituitary. For the purpose to analyze the role of these non-pituitary hormones in mammary cells, $\beta$ -lactoglobulin (BLG) gene promoter was selected as a model system. The growth hormone suppressed BLG promoter activity when it was applied alone on cultured mammary HCll cells. Along with lactogenic hormones such as insulin, prolactin and glucocorticoid, however, it significantly enhanced expression of BLG promoter activity in a dosage- dependent manner. Exogenous expression of the growth hormone gene in cultured mammary cells also strongly promoted cell proliferation and BLG promoter activity. Bovine growth hormone promoter, on the contrary, did not revealed any notable activity. Above results suggest that endogenous expression of the pituitary hormone genes in mammary cells is not a regulation leakage but a physiological control. Moreover, artificial overproduction of the growth hormone in mammary gland may help increase milk production.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.48 no.3
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• pp.346-353
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• 2015

Glucocorticoids (GCs) are steroid hormones regulated through responses to stress to maintain diverse metabolic and homeostatic functions. GCs act on the glucocorticoid receptor (GR), a member of the nuclear receptor family. This study identified and characterized the GR gene from the big-belly seahorse Hippocampus abdominalis designating it HaGR. The open reading frame of the HaGR cDNA was 2,346 bp in length, encoding a 782-amino-acid polypeptide with a theoretical isoelectric point of 6.26 and predicted molecular mass of 86.8 kDa. Nuclear receptors share a common structural organization, comprising an N-terminal transactivation domain, DNA-binding domain, and C-terminal ligand-binding domain. The tissue-specific mRNA expression profile of HaGR was analyzed in healthy seahorses using a qPCR technique. HaGR mRNA was expressed ubiquitously in all of the tissues examined, with the highest expression levels in kidney, intestine, stomach, and gill tissues. The mRNA expression in response to immune challenge with lipopolysaccharide (LPS), polyinosinic:polycytidylic acid (poly I:C), Edwardsiella tarda, and Streptococcus iniae revealed that it is inducible in response to pathogen infection. These results suggest that HaGR is involved in the immune response of the big-belly seahorse.

• Tuberculosis and Respiratory Diseases
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• v.54 no.4
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• pp.439-448
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• 2003

Background : Surfactant protein B(SP-B) and surfactant protein C(SP-C) are important in accelerating surface spreading of surfactant phospholipid. The glucocorticoids accelerate the morphologic differentiation of epithelial cells into type II cells and increase the rate of phosphatidylcholine synthesis. The hydrophobic surfactant protein has been shown to be upregulated by glucocorticoids in vitro, however, its regulation in vivo is not well established. Methods : The authors investigated the effects of glucocorticoid on the accumulation of mRNA encoding SP-B and SP-C protein content of the lung. Adult rats were given different doses of subcutaneous dexamethasone and sacrificed at 24 hours and 1 week. SP-B and SP-C mRNA were measured by a filter hybridization method. Results : 1) The accumulation of SP-B mRNA at 24 hours after 0.2 mg/kg dexamethasone treatment was increased by 23.7%. 2) The accumulation of SP-B mRNA at 1 week after 2 mg/kg dexamethasone treatment was significantly increased by 96.6%(P<0.001). 3) The accumulation of SP-C mRNA at 24 hours after 0.2 mg/kg dexamethasone treatment was significantly increased by 42.7%(P<0.01). 4) The accumulation of SP-C mRNA at 1 week after 2 mg/kg dexamethasone treatment was significantly increased by 60.0% (P<0.01). Conclusion : The authors concluded that dexamethasone treatment in vivo resulted in increased levels of SP-B mRNA and SP-C mRNA. These results suggested that dexamethasone stimulates the synthesis of hydrophobic proteins associated with surfactant.

• Journal of Korean Biological Nursing Science
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• v.25 no.1
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• pp.280-320
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• 2023

Purpose: This study was conducted to assess the antidepressant effects of capsaicin in chronic depressive rats and elucidate the mechanism underlying its effects. Methods: Male Wistar rats (280~320 g, 8 weeks of age) were subjected to depression induced by chronic unpredictable mild stresses. The rats were exposed to 8 kinds of stresses for 8 weeks. In the last 2 weeks, fluoxetine or capsaicin was injected subcutaneously. The dose of fluoxetine was 10 mg/kg (body weight), while the doses of capsaicin consisted of low (1 mg/kg), middle (5 mg/kg), and high (10 mg/kg). The forced swim test (FST) was conducted to evaluate the immobility time of rats. The immobility time indicates despair, one of symptoms of depression. The change of tryptophan hydroxylase (TPH) in the dorsal raphe was investigated using immunohistochemistry. In the hippocampus cornu ammonis (CA) 1 and 3, glucocorticoid receptor (GR) expression was measured. Results: The immobility time in the FST was significantly lower (p < .05) in the low-dose (M = 32.40 ± 13.41 seconds) and middle-dose (M = 28.48 ± 19.57 seconds) groups than in the non-treated depressive rats (M = 90.19 ± 45.34 seconds). The amount of TPH in the dorsal raphe was significantly higher (p < .05) in the middle-dose (M = 249.17 ± 35.02) and high-dose (M = 251.0 ± 56.85) groups than in the non-treated depressive rats (M = 159.78 ± 41.16). However, GR expression in the hippocampus CA1 and CA3 did not show significant differences between the non-treated depressive rats and the capsaicin-injected rats. Conclusion: This study suggests that capsaicin produces an antidepressant-like effect on chronic unpredictable mild stress-induced depression in rats via the serotonin biosynthesis pathway.

• Journal of Life Science
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• v.32 no.3
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• pp.256-262
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• 2022

Oxysterols are oxygenated metabolites of cholesterol generated by serial enzymatic reactions during bile acid synthesis. Similar to cholesterol, oxysterols move rapidly to the intracellular region and modulate various cellular processes, such as immune cell responses, lipid metabolism, and cholesterol homeostasis. Different nuclear transcription factors, such as glucocorticoid, estrogen, and liver X receptors, can be modulated by oxysterols in multiple tissues. The most abundant oxysterol, 27-hydroxycholesterol (27-OHC), is a well-known selective modulator that can either activate or suppress estrogen receptor activity in a tissue-specific manner. The contribution of 27-OHC in atherosclerosis development is apparent because a large amount of it is found in atherosclerotic plaques, accelerating the transformation of macrophages into foam cells that uptake extracellular modified lipids. According to previous studies, however, there are opposing opinions about how 27-OHC affects lipid and cholesterol metabolism in metabolic organs, including the liver and adipose tissue. In particular, the effects of 27-OHC on lipid metabolism are entirely different between in vitro and in vivo conditions, suggesting that understanding the physiology of this oxysterol requires a sophisticated approach. This review summarizes the potential effects of 27-OHC in atherosclerosis and metabolic syndromes with a special discussion of its role in metabolic tissues.