BACKGROUND: It has been already known that each trophic hormone in combined pituitary responsiveness according to gender and age brings about variable response, but in Korea, there has been no actual data. In this study, in order to assess the pituitary responsiveness, a combined pituitary stimulation test was performed in Korean subjects with the variation in CRH, GHRH, GnRH, and TRH according to their age and gender. Were these the variables that were changed according to age and gender? Clarify that. Also, it might be good to write out the abbreviations.) METHOD: Fourteen physically and mentally healthy male subjects and fourteen female subjects, also physically and mentally healthy, underwent the combined anterior pituitary stimulation test by CRH, GHRH, LHRH, and TRH. Each gender group was divided further into young(meanSE; male: 231, female: 221) and old (mean; male: 513, female: 522) groups. RESULTS: There were significant differences between the gender and age groups. The Peak GH level and maximal GH increment were significantly increased in young men compared to old men. The Peak ACTH level and maximal ACTH increment were significantly increased in old men as opposed to young men. The Peak PRL level, maximal PRL increment, Peak TSH level, and maximal TSH increment were significantly increased in old women compared to old men. The Peak FSH level was significantly increased in the two old groups compared to the young groups, which showedindependence in gender, and the maximal FSH increment was significantly increased in old men when compared with the young men. CONCLUSION: These results show that in order to for accurate interpretation of the response from the combined pituitary stimulation test, it is necessary to consider age and gender of the subjects. We suggest response values of the combined pituitary stimulation test in terms of age and gender in healthy Korean subjects.
Adrenocorticotropic Hormone ; Corticotropin-Releasing Hormone ; Female ; Gonadotropin-Releasing Hormone* ; Growth Hormone-Releasing Hormone ; Humans* ; Korea ; Male

No abstract available.
Amniotic Fluid* ; Corticotropin-Releasing Hormone* ; Female ; Obstetric Labor, Premature* ; Pregnancy

No abstract available.
Animals ; Corticotropin-Releasing Hormone* ; Dogs* ; Hypothalamus* ; Neurons* ; Somatostatin*

Animals ; Mice ; Corticotropin-Releasing Hormone/metabolism* ; Neurons/metabolism* ; Brain/metabolism*

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.
Cell Movement* ; Corticotropin-Releasing Hormone* ; Homicide ; Humans* ; Immunity, Innate ; Killer Cells, Natural* ; Lymphocytes ; Receptors, Corticotropin-Releasing Hormone

OBJECTIVES: Corticotropin releasing factor (CRF) plays a primary role in coordinating the neuroendocrine, autonomic, immune and behavioral responses to stress. CRF exerts its action through two major receptors, corticotropin-releasing factor 1 Receptor (CRF-R1) and corticotropin-releasing factor 2 receptor (CRF-R2). Using two types of chronic stress models, we investigated the changes of CRF-R1 mRNA and CRF-R2A mRNA expressions and CRF mRNA in the stress related brain circuit areas. METHODS: Male Sprague-Dawley rats were exposed to either immobilization stress or variable intermittent unpredictable stress for 10 days and then in situ hybridization histochemistry was used to quantify CRF expression in the brain. RESULTS: 1) CRF1 receptor mRNA expressions were decreased in bed nucleus stria terminalis (BNST) following stressors. 2) CRF2A receptor mRNA expressions were increased in lateral septum following stressors. 3) CRF mRNA expressions were increased in central nucleus of amygdala (CeA) and BNST. CONCLUSION: The increased CRF mRNA of CeA and BNST may be related with anxiety response in the repeated stress. Down-regulation of CRF-R1 mRNA expression in BNST may represent a compensatory adaptation to chronic stress and may be involved in the anxiety response, whereas up-regulation of CRF-R2A mRNA expression in lateral septum may represent an anxiety response or impaired learning but the functional meaning is uncertain.
Adrenocorticotropic Hormone* ; Amygdala ; Anxiety ; Brain ; Corticotropin-Releasing Hormone* ; Down-Regulation ; Humans ; Immobilization ; In Situ Hybridization ; Learning ; Male ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone ; RNA, Messenger ; Up-Regulation

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-1beta(IL-1beta). 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.
Brain ; Central Nervous System ; Corticotropin-Releasing Hormone* ; Macrophages ; Neurodegenerative Diseases ; Neuropeptides ; Nitric Oxide* ; Receptors, Corticotropin-Releasing Hormone ; RNA, Messenger ; Tumor Necrosis Factor-alpha

Functional dyspepsia (FD) and irritable bowel syndrome (IBS) are common gastrointestinal (GI) diseases; however, there is frequent overlap between FD and IBS patients. Emerging evidence links the activation of corticotropin releasing factor (CRF) receptors with stress-related alterations of gastric and colonic motor function. Therefore, we investigated the effect of peripheral CRF peptide and water avoidance stress (WAS) on upper and lower GI transit in guinea pigs. Dosages 1, 3, and 10 µg/kg of CRF were injected intraperitoneally (IP) in fasted guinea pigs 30 minutes prior to the intragastric administration of charcoal mix to measure upper GI transit. Colonic transits in non-fasted guinea pigs were assessed by fecal pellet output assay after above IP CRF doses. Blockade of CRF receptors by Astressin, and its effect on GI transit was also analyzed. Guinea pigs were subjected to WAS to measure gastrocolonic transit in different sets of experiments. Dose 10 µg/kg of CRF significantly inhibited upper GI transit. In contrast, there was dose dependent acceleration of the colonic transit. Remarkably, pretreatment of astressin significantly reverses the effect of CRF peptide on GI transit. WAS significantly increase colonic transit, but failed to accelerate upper GI transit. Peripheral CRF peptide significantly suppressed upper GI transit and accelerated colon transit, while central CRF involved WAS stimulated only colonic transit. Therefore, peripheral CRF could be utilized to establish the animal model of overlap syndrome.
Acceleration ; Animals ; Charcoal ; Colon* ; Corticotropin-Releasing Hormone ; Dyspepsia ; Guinea Pigs* ; Guinea* ; Humans ; Irritable Bowel Syndrome ; Models, Animal ; Receptors, Corticotropin-Releasing Hormone ; Water*

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.
Cell Line* ; Cell Migration Assays ; Cell Movement* ; Corticotropin-Releasing Hormone* ; Humans* ; Neoplasm Metastasis ; Oxidative Stress ; Receptors, Corticotropin-Releasing Hormone ; Stomach Neoplasms*

High-altitude hypoxia can induce physiological dysfunction and mountain sickness, but the underlying mechanism is not fully understood. Corticotrophin-releasing factor (CRF) and CRF type-i receptors (CRFR1) are members of the CRF family and the essential controllers of the physiological activity of the hypothalamo-pituitary-adrenal (HPA) axis and modulators of endocrine and behavioral activity in response to various stressors. We have previously found that high-altitude hypoxia induces disorders of the brain-endocrine-immune network through activation of CRF and CRFR1 in the brain and periphery that include activation of the HPA axis in a time- and dose-dependent manner, impaired or improved learning and memory, and anxiety-like behavioral change. Meanwhile, hypoxia induces dysfunctions of the hypothalamo-pituitary-endocrine and immune systems, including suppression of growth and development, as well as inhibition of reproductive, metabolic and immune functions. In contrast, the small mammals that live on the Qinghai-Tibet Plateau alpine meadow display low responsiveness to extreme high-altitude-hypoxia challenge, suggesting well-acclimatized genes and a physiological strategy that developed during evolution through interactions between the genes and environment. All the findings provide evidence for understanding the neuroendocrine mechanisms of hypoxia-induced physiological dysfunction. This review extends these findings.
Altitude ; Animals ; Brain ; physiopathology ; Corticotropin-Releasing Hormone ; metabolism ; Hypothalamo-Hypophyseal System ; physiopathology ; Hypoxia ; physiopathology ; Pituitary-Adrenal System ; physiopathology ; Receptors, Corticotropin-Releasing Hormone ; metabolism ; Tibet