Kyung-Eun Kim

Sookmyung Women's University, Sŏul, Seoul, South Korea

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Publications (7)23.77 Total impact

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    ABSTRACT: The erythroid differentiation regulator 1 (Erdr1), which is a novel and highly conserved factor, was recently reported to be negatively regulated by IL-18 and to play a crucial role as an antimetastatic factor. IL-18 is a proinflammatory cytokine that functions as an angiogenic mediator in inflammation. Rosacea is a chronic inflammatory skin disorder that is characterized by abnormal inflammation and vascular hyperactivity of the facial skin. To determine whether Erdr1 contributes to the regulation of the chronic inflammatory process in the development of rosacea, an immunohistochemical analysis was performed in healthy donors and patients with rosacea. In this study, we showed that Erdr1 was downregulated, whereas IL-18 was upregulated, in patients with rosacea, which led us to question the role of Erdr1 in this disorder. Moreover, a rosacea-like BALB/c mouse model was used to determine the role of Erdr1 in rosacea in vivo. LL-37 injection induced typical rosacea features, including erythema, telangiectasia, and inflammation. Treatment with recombinant Erdr1 (rErdr1) resulted in a significant reduction of erythema, inflammatory cell infiltration (including CD4(+) and CD8(+) T cells), and microvessel density with vascular endothelial growth factor (VEGF). Taken together, our findings suggest that rErdr1 may be involved in attenuating the inflammation and angiogenesis associated with the pathogenesis of rosacea. Thus, these results provide new insight into the mechanism involved in this condition, and indicate that rErdr1 could be a potential target for therapeutic intervention of rosacea. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · May 2015 · Experimental Dermatology
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    ABSTRACT: Interleukin-18 (IL-18) has recently been shown to have a pro-cancer effect in various cancers. Increased serum levels of both IL-18 and transferrin in cancer patients are correlated with its malignancy. However, the relationship between transferrin and IL-18 is not well understood. Here, we show that exogenous transferrin enhanced breast cancer cell proliferation and the proliferation rate was reduced when endogenous transferrin expression was inhibited by transferrin siRNA. The expression of endogenous transferrin was found to be regulated by IL-18. Furthermore, we found that the MAPK pathway is involved in IL-18-induced transferrin production. In conclusion, IL-18 is suggested as an inducer of endogenous transferrin expression in breast cancer cells.
    No preview · Article · Jul 2009 · Cancer letters
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    ABSTRACT: Thymosin beta 4 (T beta 4), which is the major G-actin sequestering protein, has been shown to have ubiquitous distribution and multiple biological activities. However, T beta 4's functions in relation to natural killer(NK) cells are still unknown. In this study, we show that synthetic T beta 4 peptide increases NK cell cytotoxicity mediated by intercellular adhesion molecule-1 (ICAM-1) through the secretion of cytolytic granules to target cells. This suggests that T beta 4 is a key activator of NK cell cytotoxicity.
    No preview · Article · Apr 2009 · Immunology letters
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    ABSTRACT: IL-18 has recently been reported to play a critical role in tumor migration, invasion, and metastasis. Because IL-18 has various biological activities after its secretion as an 18 kDa mature form, the regulation of the IL-18 secretion process is an important step in tumor progression. This study investigated the implication of IL-18 in vascular endothelial growth factor (VEGF)-D-regulated migration, along with the role of the IL-18 secretion process. VEGF-D enhanced cell migration, which was then blocked by inhibiting IL-18. VEGF-D increased IL-18 expression and secretion, suggesting that IL-18 is a critical mediator for VEGF-D-enhanced migration. VEGF-D induced a disintegrin and metalloprotease 33 (ADAM33) expression, which has a metalloproteinase domain. VEGF-D-enhanced IL-18 secretion and cell migration were inhibited by ADAM33 knock-down. Moreover, cell proliferation was considerably reduced in ADAM33 small interfering RNA transfectants. In conclusion, ADAM33 has a key role in gastric cancer pathogenesis by up-regulating IL-18 secretion process, resulting in increased cell migration and proliferation.
    Full-text · Article · Apr 2009 · The Journal of Immunology
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    ABSTRACT: Expression of UL16-binding proteins (ULBPs) has been reported in various cancers, such as leukemia and melanoma, and also in some other cancer cell lines. However, the factors that modulate the expression of ULBPs are not well defined. In this study, we investigated the effects of IL-18 on the expression of NKG2D ligands in leukemia cells. IL-18 treatment increased ULBP2 expression in leukemia cells at the mRNA and protein levels. In addition, PD98059 (an ERK1/2 MAPK inhibitor) and SP600125 (a JNK inhibitor) attenuated IL-18-induced ULBP2 expression in a dose-dependent manner. We observed that ERK1/2 and JNK MAPK phosphorylation increased upon treatment with IL-18. IL-18 elevated CD107a expression in cancer cells and increased the cytotoxic activity of NK cells; therefore, we propose that IL-18 increases the susceptibility of target cells by inducing surface expression of ULBP2. Taken together, these findings suggest that IL-18 may play a critical role in regulating ULBP2 expression via the ERK1/2 and JNK MAPK pathways in leukemia cells.
    No preview · Article · Oct 2008 · Immunology Letters
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    ABSTRACT: Interleukin-18 (IL-18) has multiple effects on various cells that are involved in immune escape of murine melanoma cells and in the inflammatory responses. This study investigated the effect of IL-18 on the ability of murine melanoma cells to migrate by using B16F10 cells and the IL-18 antisense transfectants of B16F10 cells (the B16F10/IL-18 antisense transfectant). The B16F10 cells were more able to migrate than were the B16F10/IL-18 antisense transfectants. An exogenous IL-18 treatment improved the ability of the B16F10/IL-18 antisense transfectant cells to migrate, indicating that IL-18 enhanced the migration ability of melanoma cells. To determine the signaling mechanisms involved in IL-18-enhanced migration, we measured the ROI levels. It was found that the ROI levels were increased by IL-18, and an antioxidant, N-acetyl-l-cystein (NAC), blocked the effect of IL-18 on migration, suggesting the involvement of ROI in the signal transduction of IL-18-enhanced cell migration. IL-18-enhanced cell migration was also reduced by PD98059. In addition, the level of ERK1/2 phosphorylation was markedly increased by treating with exogenous IL-18 at 20 min. These results suggest that IL-18 enhances the ability of melanoma cells to migrate via the generation of ROI and the MAPK pathway.
    No preview · Article · Dec 2006 · Immunology Letters
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    ABSTRACT: TGF-beta is known to play a major role for the reduced NKG2D expression seen in cancer patients. However, the mechanisms for reduced TGF-beta-induced down-regulation of NKG2D are unclear. In this study, we observed that IL-2/IL-18 increased the NKG2D expression in the TGF-beta treated NK cell line in a dose-dependent manner. Incubation with the JNK inhibitor SP600125 inhibited the NKG2D expression induced by IL-2/IL-18 in the TGF-beta treated human NK cell line. Moreover, the NK cytotoxicity assay showed that the reduced NK cytotoxicity by TGF-beta was recovered by IL-2/IL-18 treatment. The results indicate that IL-2/IL-18 strongly prevented the TGF-beta-induced NKG2D down-regulation in NK cells via the JNK pathway. Taken together, the protected expression of NKG2D by IL-2/IL-18 provides insight into the mechanism of NKG2D regulation and it also supplied useful information for creating a novel therapeutic approach to treat TGF-beta-secreting cancer cells.
    No preview · Article · Aug 2006 · Cellular Immunology

Publication Stats

101 Citations
23.77 Total Impact Points


  • 2006-2015
    • Sookmyung Women's University
      • Department of Biological Science
      Sŏul, Seoul, South Korea