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Regulation of IL-18 expression by CRH in mouse microglial cells
Yang, Yoolhee,Hahm, Eunsil,Kim, Youngin,Kang, Jaeseung,Lee, Wangjae,Han, Innoc,Myung, Pyungkeun,Kang, Hyungsik,Park, Hyunjeong,Cho, Daeho 충남대학교 형질전환복제돼지연구센터 2004 논문집 Vol. No.8
Corticotropin Releasing Hormone (CRH) is a major regulator of the stress response. This study examined whether CRH regulates interleukin-18 expression on microglia, BV2. Our data show that CRH enhanced IL-18 expression and significantly induced the secretion of functional IL-18 protein. Furthermore, CRH induced IL-18 production could be blocked by N-acetyl-L-cystein (NAC), which suggests that reactive oxygen intermediates (ROI) may be involved in regulating IL-18. Indeed, it was also found that CRH increased the generation of ROI. Taken together, these results indicate that CRH is an important mediator that regulates IL-18 expression in the brain during stress.
Regulation of IL-18 expression by CRH in mouse microglial cells
Yang, Yoolhee,Hahm, Eunsil,Kim, Youngin,Kang, Jaeseung,Lee, Wangjae,Han, Innoc,Myung, Pyungkeun,Kang, Hyungsik,Park, Hyunjeong,Cho, Daeho 충남대학교 형질전환복제돼지연구센터 2007 논문집 Vol. No.10
Corticotropin releasing hormone (CRH) is a major regulator of the stress response. This study examined whether CRH regulates interleukin-18 expression on microglia, BV2. Our data show that CRH enhanced IL-18 expression and significantly induced the secretion of functional IL-18 protein. Furthermore, CRH induced IL-18 production could be blocked by N-acetyl-L-cystein (NAC), which suggests that reactive oxygen intermediates (ROI) may be involved in regulating IL-I8. Indeed, it was also found that CRH increased the generation of ROJ. Taken together, these results indicate that CRH is an important mediator that regulates IL-18 expression in the brain during stress.
Yang, Yoolhee,Park, Hyunjeong,Yang, Young,Kim, Tae Sung,Bang, Sa Ik,Cho, Daeho Munksgaard 2007 Experimental Dermatology Vol.16 No.1
<P>Abstract: </P><P>Melanoma is a malignant skin cancer that displays a high rate of tumor cell migration and metastasis. This study examined how corticotropin-releasing hormone (CRH) affects the migration of melanoma cells in order to further understand the relationship between stress and tumor cell migration. The migration assay data showed that CRH treatment increased the level of B16F10 cell migration in a dose- and time-dependent manner. To determine whether the extracellular signal-regulated protein kinase 1/2 (ERK1/2) signaling pathway is involved in the upregulation of melanoma migration, cells were pretreated with an inhibitor of ERK1/2 (PD098059). The pretreatment of PD098059 blocked the increase in cell migration. Furthermore, CRH induced the phosphorylation of ERK1/2. The maximum activation of ERK1/2 by CRH was observed at 15 min. Taken together, these results suggest that CRH is an important mediator that regulates the migration of melanoma cells in the skin during stress through the ERK1/2 signaling pathway.</P>
김태선,양을희,김판기 용인대학교 자연과학연구소 1998 自然科學硏究所論文誌 Vol.3 No.1
This study was carried out to determine the adequacy of drinking water in school cafeteria for potable water. In this study, total coliforms and total bacteria were included. For this study, three samples was used and collected two times from each places during from september 22 to 27. The following results were obtained : In school cafeteria A and C, the total coliform group was detected below 3MPN/100ml and total bacteria was below the drinking water standard. In this study, microbiological examination were showed that drinking water was adequacy. In contrast with the school cafeteria A and C, the total coliform group was 3.6 MPN/100ml(T.C.) and total bacteria was 165cfu/ml in the school cafeteria B. The range of 95% confidence limits,the total coliform group was from minimum 0.5/100ml to maximum 20/100ml. School cafeteria B was exceed in Korea water quility acceptable limit, and was required of careful management.
Erythroid differentiation regulator 1 (Erdr1) is a proapototic factor in human keratinocytes
Kim, Hee Jung,Song, Seok Bean,Yang, Yoolhee,Eun, Young Sun,Cho, Baik Kee,Park, Hyun Jeong,Cho, Dae Ho Blackwell Publishing Ltd 2011 Experimental dermatology Vol.20 No.11
<P><B>Abstract: </B> Skin is constantly exposed to physical and chemical stressors. The exposure of keratinocytes to ultraviolet B (UVB) irradiation causes epidermal damage via induction of apoptosis. Erythroid differentiation regulator 1 (Erdr1) modulates growth and survival of cells under various stressful conditions, but the function of Erdr1 in human keratinocyte apoptosis has not been investigated so far. Here, we investigated the effect of Erdr1 on UVB‐induced apoptosis in human keratinocytes and also examined the underlying regulatory mechanism. First, Erdr1 expression was detected in human primary keratinocytes and normal human skin tissues. Expression of Erdr1 was enhanced in human keratinocytes following UVB irradiation. Knock‐down of Erdr1 led to resistance to UVB‐induced apoptosis. Also, Erdr1 overexpression increased UVB‐induced apoptosis and induced caspase‐3 activation. Furthermore, the extracellular signal‐regulated kinase (ERK) inhibitor PD98059 and the p38 mitogen‐activated protein kinase (MAPK) inhibitor SB203580 significantly reduced Erdr1 expression following UVB irradiation. These results indicate that UVB induces Erdr1 via a MAPK‐dependent mechanism. Taken together, these findings suggest that Erdr1 has a role as a proapoptotic factor in human keratinocytes and acts via ERK and p38 MAPK pathways. Therefore, Erdr1 may be a potential therapeutic target to reduce apoptosis in keratinocytes in conditions such as psoriasis and skin cancer.</P>
Erdr1 Attenuates Dermatophagoides farina Body Extract-Induced Atopic Dermatitis in NC/Nga Mice
Kim, Kyung Eun,Jung, Myung Jin,Houh, Younkyung,Kim, Tae Sung,Lee, Wang Jae,Yang, Yoolhee,Bang, Sa Ik,Kim, Chang Han,Kim, Heejong,Park, Hyun Jeong,Cho, Daeho Williams & Wilkins 2017 The Journal of investigative dermatology Vol.137 No.8
Cho, Daeho,Kang, Jae Seung,Park, Jong Hoon,Kim, Young-In,Hahm, Eunsil,Lee, Junechul,Yang, Yoolhee,Jeon, Junho,Song, HyunKeun,Park, Hyunjeong,Kim, Taesung,Pang, Saic,Kim, Chul-Woo,Hwang, Young Il,Lee, 전남대학교 약품개발연구소 2002 약품개발연구지 Vol.11 No.-
Based on our recent observation that enhanced IL-18 expression positively correlates with malignant skin tumors, such as SCC and melanoma, we examined the possible role of UVB, known to be associated with skin cancer development, in the enhancement of IL-18 production using primary human epidermal keratinocytes and human cell line HaCaT. After cells were exposed to UVB irradiation in vitro, IL-18 production was examined by Northern blot analysis and ELISA, and it was found that IL-18 production is enhanced by UVB irradiation in a dose- and time-dependent manner. In addition, we confirmed that it is functionally active form of IL-18 using the inhibitor of caspase-1. The effect of UVB irradiation was blocked by antioxidant, N-acetyl-ι-cysteine (NAC), which suggested the involvement of reactive oxygen intermediates (ROI) in the signal transduction of UVB irradiation-enhanced IL-18 synthesis. We also found that UVB irradiation increased AP-1 binding activity by using EMSA with AP-1-specific oligonucleotide. Furthermore, inhibitors of UVB-induced AP-1 activity, such as PD98059, blocked enhanced IL-18 production, indicating that AP-1 activation is required for UVB-induced IL-18 production. Taken together, our results suggest that UVB irradiation-enhanced IL-18 production is selectively mediated through the generation of ROI and the activation of AP-1.
The Effects of Artemisinin on the Cytolytic Activity of Natural Killer (NK) Cells
Houh, Youn Kyung,Kim, Kyung Eun,Park, Sunyoung,Hur, Dae Young,Kim, Seonghan,Kim, Daejin,Bang, Sa Ik,Yang, Yoolhee,Park, Hyun Jeong,Cho, Daeho MDPI 2017 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.18 No.7
<P>Artemisinin, a chemical compound used for the treatment of malaria, has been known to show anti-cancer activity. However, the effect of this chemical on natural killer (NK) cells, which are involved in tumor killing, remains unknown. Here, we demonstrate that artemisinin exerts a potent anti-cancer effect by activating NK cells. NK-92MI cells pre-treated with artemisinin were subjected to a cytotoxicity assay using K562 cells. The results showed that artemisinin significantly enhances the cytolytic activity of NK cells in a dose-dependent manner. Additionally, the artemisinin-enhanced cytotoxic effect of NK-92MI cells on tumor cells was accompanied by the stimulation of granule exocytosis, as evidenced by the detection of CD107a expression in NK cells. Moreover, this enhancement of cytotoxicity by artemisinin was also observed in human primary NK cells from peripheral blood. Our results suggest that artemisinin enhances human NK cell cytotoxicity and degranulation. This is the first evidence that artemisinin exerts antitumor activity by enhancing NK cytotoxicity. Therefore, these results provide a deeper understanding of the action of artemisinin and will contribute to the development and application of this class of compounds in cancer treatment strategies.</P>
Park, Yoorim,Jung, Min Kyung,Yoon, Sun Young,Lee, Ha-Reum,Hur, Dae Young,Kim, Daejin,Yang, Yoolhee,Kim, Tae Sung,Kim, Seonghan,Yoon, Suk Ran,Park, Hyun Jeong,Bang, Sa Ik,Cho, Dae Ho Published for the International Union of Biochemis 2013 Biotechnology and applied biochemistry Vol.60 No.3
<P>Adipose stem cells (ASCs) are pluripotent cells that can generate pure fat tissue for regeneration. Differentiated adipose cells have been generated by a common inducer cocktail composed of dexamethasone, insulin, and isobutylmethylxanthine (DIM). The major drawbacks of adipose cells are their tendency to float on the culture media and their cost. To overcome some of these disadvantages, a new inducer cocktail that includes insulin, dehydroepiandrosterone, and histamine (DH IH) was tested. As a result, lipid accumulation was elevated more than twofold with DH IH than with DIM. Cell adhesion and viability, which are important factors for stable differentiation, were increased with DH IH and were proven through measurement of mRNA expression levels of adhesion marker genes, N-cadherin and vascular cell adhesion molecule, as well as through an alamar blue assay. The expression of adipogenesis-related genes, adiponectin, and glucose transporter type 4 lasted for a long time. To improve the efficiency of grafting, cell adhesion and neovascularization need to be increased. Neovascularization was observed around the transplanted adipose cells, which showed a higher number of vessel formation in DH IH than in DIM. The above results suggest that DH IH can produce pure differentiated adipose cells effectively and enhance their adhesion onto the target location when these differentiated adipose cells were applied as a clinical resource.</P>