• 제목/요약/키워드: corticotropin-releasing hormone

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Protein-Protein Interaction Analysis of Corticotropin - Releasing Hormone Receptor 1 with Corticotropin-Releasing Hormone and Sauvagine

  • Nagarajan, Santhosh Kumar
    • 통합자연과학논문집
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    • 제11권2호
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    • pp.101-106
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    • 2018
  • Corticotropin - releasing hormone receptor 1 (CRHR1) forms an integral part of the pathophysiology of disorders like post-traumatic stress disorder, stress, anxiety, addiction, and depression. Hence it is essential to look for new, potent and structure-specific inhibitors of CRHR1. We have analysed the protein-protein interaction complexes of the CRHR1 receptor with its native ligand CRF and full agonist Sauvagine. The structure of Sauvagine was predicted using homology modelling. We have identified that the residues TYR253, ASP254, GLU256, GLY265, ARG1014 and LY1060 are important in the formation of protein-protein complex formation. Future studies on these residues could throw light on the crucial structural features required for the formation of CRHR1-inhibitor complex and in studies that try to solve the structural complexities of CRHR1.

Corticotropin-Releasing Hormone (CRH)에 의한 인간 위암 세포(MKN-28)의 Migration 증가 (Enhancement of Cell Migration by Corticotropin-Releasing Hormone (CRH) in Human Gastric Cancer Cell Line, MKN-28)

  • 천소영;조대호
    • IMMUNE NETWORK
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    • 제4권4호
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    • pp.244-249
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    • 2004
  • Background: Corticotropin-Releasing Hormone (CRH), an important regulator of stress response, has a potent immunoregulatory effect with the ability to promote the growth of various cancer through CRH receptor type 1 under stress. Although the metastasized cancers through cell migration are more aggressive than the primary cancers, little is known about the effect of CRH on cell migration. Gastric cancer is prone to metastasize to other tissues and it is reported that gastric cancer is response to various stresses such as oxidative stress. Herein, we studied the relationship between CRH and gastric cancer cell migration. Methods: We used gastric cancer cell line, MKN-28 and tested the CRH receptor type 1 expression on MKN-28 by RT-PCR. To examine the change in the ability of migration by CRH in MKN-28, cells were incubated with CRH and then migration ability was measured using a cell migration assay. Results: We confirmed that CRH receptor type 1 was expressed in MKN-28 and HaCaT cells. The migration ability of MKN-28 cells was increased by CRH in a time-, dose- dependent manner. Conclusion: These data suggest that CRH increases migration ability in gastric cancer cell line and that CRH may be a critical regulator in the metastasis of gastric cancer cell.

생쥐 미세아교세포(BV2)에서 Corticotropin-releasing Hormone (CRH)에 의한 Nitric Oxide (NO) 생성의 증가 (Enhancement of Nitric Oxide Production by Corticotropin-releasing Hormone (CRH) in Murine Microglial Cells, BV2)

  • 양율희;양영;조대호
    • IMMUNE NETWORK
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    • 제4권1호
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    • pp.60-64
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    • 2004
  • Background: Microglial cells, major immune effector cells in the central nervous system, become activated in neurodegenerative disorders. Activated microglial cells produce proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-$\alpha$ and interleukin-$1{\beta}$(IL-$1{\beta}$). These proinflammatory mediators have been shown to be significantly increased in the neurodegenerative disorders such as Alzhimer's disease and Pakinson's disease. It was known that one of the neurodegeneration source is stress and it is important to elucidate mechanisms of the stress response for understanding the stress-related disorders and developing improved treatments. Because one of the neuropeptide which plays a main role in regulating the stress response is corticotropin-releasing hormone (CRH), we analyzed the regulation of NO release by CRH in BV2 murine microglial cell as macrophage in the brain. Methods: First, we tested the CRH receptor expression in the mRNA levels by RT-PCR. To test the regulation of NO release by CRH, cells were treated with CRH and then NO release was measured by Griess reagent assay. Results: Our study demonstrated that CRH receptor 1 was expressed in BV2 murine microglial cells and CRH treatment enhanced NO production. Furthermore, additive effects of lipopolysaccaride (LPS) and CRH were confirmed in NO production time dependantly. Conclusion: Taken together, these data indicated that CRH is an important mediator to regulate NO release on microglial cells in the brain during stress.

Corticotropin-Releasing Hormone (CRH)에 의한 인간 자연 살해 세포(NK-92MI)의 Migration 억제 (Inhibition of Cell Migration by Corticotropin-Releasing Hormone (CRH) in Human Natural Killer Cell Line, NK-92MI)

  • 천소영;방사익;조대호
    • IMMUNE NETWORK
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    • 제5권4호
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    • pp.247-251
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    • 2005
  • Background: Natural killer (NK) cells are CD3 (-) CD14 (-) CD56 (+) lymphocytes. They play an important role in the body's innate immune response. They can induce spontaneous killing of cancer cells or virus-infected cells via the Fas/Fas ligand or the granzyme/perforin systems. The corticotropin-releasing hormone (CRH) is an important regulator for the body's stress response. It promotes proliferation and migration of various cancer cells through the CRH type 1 receptor under stress, and also inhibits NK or T cell activity. However, the relationship of CRH and NK cell migration to the target has not been confirmed. Herein, we study the effect of CRH on NK cell migration. Methods: We used the human NK cell line, NK-92MI, and tested the expression of CRH receptor type 1 on NK-92MI by RT-PCR. This was to examine the effect of CRH on tumor and NK cell migration, thus NK cells (NK-92MI) were incubated with or without CRH and then each CRH treated cell's migration ability compared to that of the CRH untreated group. Results: We confirmed that CRH receptor type 1 is expressed in NK-92MI. CRH can decrease NK cell migration in a time-/dose-dependent manner. Conclusion: These data suggest CRH can inhibit NK cell migration to target cells.

정신분열병 환자의 우울증상과 불안증상이 Dexamethasone/Corticotropin Releasing Hormone 병합검사 결과에 미치는 영향 (The Effect of Depression and Anxiety Symptoms on the Results of Combined Dexamethasone/Corticotropin Releasing Hormone Test in Patients with Schizophrenia)

  • 한병진;이상익;신철진;손정우
    • 생물정신의학
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    • 제17권2호
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    • pp.86-93
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    • 2010
  • Objectives : The aim of this research is to determine the effects of depression and anxiety symptoms of schizophrenic psychopathology on the HPA axis. Methods : Twenty patients with schizophrenia were included and divided into the medication non-exposed group(n = 10) and the medication exposed group(n = 10). Evaluated scales were the Positive and Negative Syndrome Scale(PANSS), Scale for the Assessment of Negative Symptoms(SANS), Scale for the Assessment of Positive Symptoms(SAPS), Hamilton Depression Inventory(HAM-D) and Hamilton Anxiety Inventory (HAM-A), and then the combined Dexamethasone/Corticotropin Releasing Hormone(DEX/CRH) test was conducted to determine the basal level, the peak level and the area under the curve(AUC) of cortisol and adrenocorticotropic hormone(ACTH). Results : When the correlations between each psychopathology and cortisol level or ACTH AUC value were analyzed, HAM-D showed a negative correlation, whereas HAM-A showed a positive correlation. Also, the non-depression group(HAM-D ${\leq}$ 18) showed higher cortisol and ACTH concentrations than the depression group(HAM-D > 18), and the anxiety group(HAM-A ${\geq}$ 14) showed significantly higher concentrations than the non-anxiety group(HAM-D < 14)(p < 0.05). Also, as for the comparison between the medication non-exposed group and the medication exposed group, the non-exposed group showed significantly higher cortisol and ACTH concentration than exposed group(p < 0.05). Conclusion : This study suggest that anxiety symptoms rather than depression symptoms are related to the increased activity of the HPA axis of schizophrenics.

Effect of Corticosterone on Hypothalamic Corticotropin-releasing Hormone Expression in Broiler Chicks (Gallus gallus domesticus) Fed a High Energy Diet

  • Song, Zhigang;Yuan, Lei;Jiao, Hongchao;Lin, Hai
    • Asian-Australasian Journal of Animal Sciences
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    • 제24권12호
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    • pp.1736-1743
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    • 2011
  • This paper reports the peripheral and central effect of corticosterone on feed intake and hypothalamic corticotropinreleasing hormone (CRH) gene expression in chicks fed a high energy diet. Three experiments were conducted: corticosterone was supplemented to the feed (30 mg/kg diet), injected subcutaneously (s.c., 4 mg/kg body weight) or intracerebroventricularly (i.c.v., 4 ng). The results showed that dietary corticosterone significantly increased feed intake. The s.c. corticosterone administration increased feed intake within 1 to 3 h and at 1 to 5 h after the injection. The i.c.v. corticosterone administration increased feed intake within 1 h after the injection, but not at 1 to 3 h. Dietary supplementation and s.c. injection of corticosterone decreased the CRH gene expression in the hypothalamus. Therefore, peripheral corticosterone exerted a decreased effect on hypothalamic CRH mRNA levels, and corticosterone had a stimulating effect on feed intake in broiler chicks fed a high energy diet.

Effects of intracerebroventricular injection of corticotrophin releasing factor on the gene expression of ghrelin and corticotrophin releasing factor receptors in broiler chickens

  • Cai, Yuanli;Song, Zhigang
    • Animal Bioscience
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    • 제35권12호
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    • pp.1904-1910
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    • 2022
  • Objective: This study aimed to investigate the effects of corticotropin-releasing factor (CRF) on the feed intake of broiler chickens and explore its influencing mechanism. Methods: The study included two trials. In trial 1, 32 male broiler chickens (Arbor Acres, Gallus gallus domesticus) were given ventricle buried tubes, and they were allowed to recover for 3 days. At 8:00 AM, intracerebroventricular (ICV) injection with CRF or normal saline was performed in 10-day-old broiler chickens, which were divided into the 5, 10, and 20 ㎍ and control (normal saline) groups according to the dose of CRF injection. In trial 2, chickens were divided into the 10 ㎍ and control group (physiological saline) to repeat trial 1. Results: Results of trial 1 showed that the cumulative amount of feed intake in the 10 or 20 ㎍ groups was considerably lower than that of the control group after ICV injection with CRF. The lowest amount of feed intake was obtained with the addition of 10 ㎍ of CRF. In trial 2, the expression of ghrelin in the hypothalamus injected with 10 ㎍ of CRF increased significantly, but the expression of ghrelin in various sections of the small intestine considerably decreased. The expression of CRF receptor subtypes 1 (CRFR1) in the hypothalamus and some parts of the small intestine remarkably increased, and the expression of CRF receptor subtypes 2 (CRFR2) increased only in the duodenum, whereas the expression of growth hormone secretagogue receptor (GHSR-1α) in the jejunum and ileum increased considerably after ICV injection of 10 ㎍ of CRF. Conclusion: The CRF at 10 ㎍ increased ghrelin expression in the hypothalamus and CRFR1 expression in the small intestine, and this phenomenon was related to the suppressed feed intake of broiler chickens.

쿠싱 증후군 일으킨 카르시노이드종양의 1예 보고: 코르티코트로핀분비호르몬 분비하는 종양 의증 (A Case Report of Thymic Carcinoid Tumor Associated with Cushing's Syndrome: Possible Corticotropin-Releasing Hormone Secreting Tumor)

  • 전순호;노선균;오영하;강준구;염종훈;이철범
    • Journal of Chest Surgery
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    • 제39권10호
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    • pp.795-798
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    • 2006
  • 쿠싱증후군과 연관된 흉선 carcinoid종양은 드문 질병으로 그 예후가 나쁜 것으로 알려져 있다. 그중 부신피질자극 호르몬 분비 촉진 호르몬을 생산하는 흉선 carcinoid 종양은 훨씬 더 드물다. 우리는 거대한 전방 종격동 종양을 갖고 있는 58세 여자 환자에 대해 보고하려고 한다. 환자는 흉선제거술 5개월 후 전반적인 부종과 호흡곤란으로 다시 입원하였다. 환자는 재발과 전이가 발견되었고 쿠싱증후군으로 진단 받았다.

Effect of Starving and Re-feeding on Appetite-related Genes in Olive Flounder Paralichthys olivaceus

  • Kim, Min Ju;Song, Jin Ah;Choi, Cheol Young
    • 한국해양생명과학회지
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    • 제7권1호
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    • pp.1-9
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    • 2022
  • This investigation aimed to assess the appetite response changes of olive flounder to starving and re-feeding conditions. Three different feeding groups (2 weeks feeding, fed; 2 weeks starving, starved; and 1 week starving and 1 week feeding, re-fed) were established to examine the changes in appetite-related genes for each group. The weight gain of the fish was highest for the fed group and lowest for the starving group. Based on the daily feed intake (DFI) and cumulative feed intake (CFI), overall food intake was found to increase in the re-fed group more than in the fed group from week 1 to week 2 of the experiment. Hypocretin neuropeptide precursor (HCRT) and galanin receptor 1 (GAL-R1) mRNA expression in the brain of olive flounder were decreased in the starved group. Corticotropin-releasing hormone (CRH) was decreased in all experimental groups, except for the fed group. However, overall leptin concentrations in the plasma did not change across groups. Considering the differences between this study and previous studies on starving and feeding, various factors (except the production and expression mechanisms of appetite-related factors in response to starving) are likely acting on the appetite responses of the fish. In this study, a 1-week re-feeding period induced substantial effects on appetite response when compared to a 2-week feeding period. These findings show that even if re-feeding is performed after starving, the unbalance caused by the re-feeding can affect various physiological changes in fish by feed intake efficiency.