• Korean Journal of Environment and Ecology
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• v.25 no.6
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• pp.853-860
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• 2011

We measured blood plasma parameters(cortisol, glucose, albumin) and glucocorticoid receptor(GCR) gene expression level of the Japanese eel(Anguilla japonica) exposed to an explosion noise for an hour in order to evaluate the effects of noise stress and to explore the possibility of these parameters as biomarkers on noise stress for one of this valuable aquaculture species. Plasma cortisol and glucose reached high levels with significant differences compared to the control group, whereas albumin showed a low value after 1 h of exposure. In addition, tissue distribution of GCR gene expression was studied by real-time RT-PCR of ten organs(brain, eye, gill, gonad, heart, intestine, kidney, liver, muscle and skin). Liver showed the highest level of expression in the control followed by gill, muscle and intestine. A time-course study revealed induction in liver, gill, muscle and intestine after 30 min or 1 h of noise exposure.

• Korean Journal of Ichthyology
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• v.22 no.1
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• pp.17-24
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• 2010

The present study investigated the expression of glucocorticoid receptor (GR) mRNA as a stress response during salinity changes (35, 10, and 0 psu) and water temperature changes (from $20^{\circ}C$ to $30^{\circ}C$, $1^{\circ}C$/day) in black porgy. We cloned the full-length GR cDNA from the kidney and examined its expression in the gill, kidney, and intestine by quantitative real-time PCR (QPCR) during salinity and water temperature changes. During salinity changes, the levels of GR mRNA in the gill, kidney, and intestine were highest at 0 psu, and the levels of plasma cortisol and glucose were elevated, but triiodothyronine ($T_3$) decreased. Also, during water temperature changes, the levels of GR mRNA in the gill, kidney, and intestine increased at $30^{\circ}C$. Plasma parameters also increased with an increase in water temperature. Therefore, this upregulation of GR mRNA was a good indicator of stress, such as those resulting from changes in salinity and water temperature.

• Proceedings of the Ginseng society Conference
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• 1997.05a
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• pp.14-14
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• 1997

• Journal of Life Science
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• v.24 no.12
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• pp.1356-1363
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• 2014

Ghrelin is a 28 amino acid orexigenic peptide hormone that is secreted predominantly by tX/A cells in the stomach, and it plays a major role in energy homeostasis. Activated ghrelin has an n-octanoyl group covalently linked to the hydroxyl group of the Ser3 residue, which is critical for its binding to the G-protein coupled growth hormone secretagogue receptor-1a (GHS-R1a). According to recent reports, both ghrelin and its receptor, GHS-R1a, are expressed by a variety of immune cells, including T- and B-lymphocytes, monocytes, and dendritic cells, and ghrelin stimulation of leukocytes provides a potent immunomodulatory signal controlling systemic and age-associated inflammation and thymic involution. Here, we report that ghrelin protected murine thymocytes from dexamethasone (DEX)-induced cell death both in vivo and in vitro. Subsequently, we explored the molecular mechanisms of the antiapoptotic effect of ghrelin. According to our experiments, ghrelin inhibited the expression of proapoptotic proteins via the regulation of glucocorticoid receptor (GR) phosphorylation. As a result, ghrelin inhibited the proapoptotic activation of proteins, such as Caspase-3, PARP, and Bim. These data suggest that ghrelin, through GHS-R, inhibits the pathway to apoptosis by regulation of the proapoptotic protein activation signal pathway. They provide evidence that blocking apoptosis is an essential function of ghrelin during the development of thymocytes.

• Proceedings of the Korean Society of Life Science Conference
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• 2002.09a
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• pp.89-89
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• 2002

• 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.

• 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.

• Archives of Pharmacal Research
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• v.10 no.3
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• pp.184-187
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• 1987

ln order to develope anti-inflammatory glucocorticoids for local use without systemic side-effects, ester and amide derivatives of 20$\xi$-dihydroprednisolonic acid have been prepared. When binding affinities of these compounds to glucocorticoid receptor of rat liver cytosol were compared, all a-isomer at C-20 showed higher binding affinities than the corres¬ponding $\beta$-isomer. The size of the substituents at C-21 had significant influences on binding affinities, which were related with their lipophilicity.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.23-33
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• 2018

Cushing's syndrome (CS) is a collection of symptoms caused by prolonged exposure to excess cortisol. Chronically elevated glucocorticoid (GC) levels contribute to hepatic steatosis. We hypothesized that histone deacetylase inhibitors (HDACi) could attenuate hepatic steatosis through glucocorticoid receptor (GR) acetylation in experimental CS. To induce CS, we administered adrenocorticotropic hormone (ACTH; 40 ng/kg/day) to Sprague-Dawley rats by subcutaneous infusion with osmotic mini-pumps. We administered the HDACi, sodium valproate (VPA; 0.71% w/v), in the drinking water. Treatment with the HDACi decreased steatosis and the expression of lipogenic genes in the livers of CS rats. The enrichment of GR at the promoters of the lipogenic genes, such as acetyl-CoA carboxylase (Acc), fatty acid synthase (Fasn), and sterol regulatory element binding protein 1c (Srebp1c), was markedly decreased by VPA. Pan-HDACi and an HDAC class I-specific inhibitor, but not an HDAC class II a-specific inhibitor, attenuated dexamethasone (DEX)-induced lipogenesis in HepG2 cells. The transcriptional activity of Fasn was decreased by pretreatment with VPA. In addition, pretreatment with VPA decreased DEX-induced binding of GR to the glucocorticoid response element (GRE). Treatment with VPA increased the acetylation of GR in ACTH-infused rats and DEX-induced HepG2 cells. Taken together, these results indicate that HDAC inhibition attenuates hepatic steatosis through GR acetylation in experimental CS.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.42 no.2
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• pp.163-171
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• 2016

Steroid hormone, glucocorticoid (GC) has strong anti-inflammatory effects by binding to glucocorticoid receptor (GR) inhibiting the expression of inflammatory genes. Therefore, agents that activate the GR have been used for the treatment of dermatitis. However, the agents have side effects such as skin barrier dysfunction and dermal atrophy, inducing skin damage as well as skin aging. It has been reported that GC is activated by 11 beta-hydroxysteroid dehydrogenase type 1 ($11{\beta}$-HSD1) to increase the activity of the GR. This study aimed to identify natural materials that can effectively inhibit dexamethasone. We found that alpinetin isolated from Alpinia katsumadai extract has a significant effect on this. Alpinetin not only inhibited $11{\beta}$-HSD1 expression, but also suppressed the increase of phosphorylated GR and cortisol concentration. Alpinetin also recovered collagen expression in dexamethasone-treated dermal fibroblasts, and the reduction of dermal thickness in dexamethasnone-treated 3D skin model. These results suggest that alpinetin prevents skin aging induced by the increase of $11{\beta}$-HSD1 expression.