http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Chemotactic effect of S100A8 and S100A9 on human eosinophilic leukemia cells, EoL-1 through TLR4
Ayoung Gu,Da Hye Kim,Na Rae Lee,In Sik Kim,이지숙 대한독성 유전단백체 학회 2018 Molecular & cellular toxicology Vol.14 No.3
Backgrounds: S100A8 and S100A9 function as key factors in inflammatory responses including cell survival, differentiation and chemotactic activity. Chronic eosinophilic leukemia (CEL) is a rare hematological malignancy with eosinophilia. Methods: In this study, we investigated the contribution of S100A8 and S100A9 to chemotaxis of the human eosinophilic leukemia cell line, EoL-1. A chemotaxis assay, western blot analysis and a NF-κB transcription factor assay were conducted to investigate the chemotactic mechanism. Results: S100A8 and S100A9 induced the migration of EoL-1 cells via the phosphorylation of PKCδ, AKT, and MAPKs and the translocation of NF-κB; however, they had no effect on eosinophils from normal peripheral blood. PKCδ, AKT, and MAPKs such as ERK, p38 MAPK, and JNK are upstream regulator molecules of NF-κB activation. Iκ-Bα degradation is needed for NF-κB activation. Conclusion: These findings suggest that S100A8 and S100A9 induce the cell movement and contribute to an understanding of S100A8 and S100A9 in eosinophil biology and the pathogenic mechanism of hematological malignancy.
The Role of S100A8 and S100A9 in Differentiation of Human Eosinophilic Leukemia Cells, EoL-1
In Sik Kim,Ayoung Gu,Ji-Sook Lee 대한의생명과학회 2017 Biomedical Science Letters Vol.23 No.1
S100A8 and S100A9 are associated with myeloid cell differentiation, chemotactic activities, adhesion of neutrophils, and apoptosis. In this study, we investigated the contribution of S100A8 and S100A9 to differentiation of the human eosinophilic leukemia cell line, EoL-1. S100A8 and S100A9 increased the number of vacuole per one cell and the protein expression of EPO and MBP. Rottlerin, an inhibitor of protein kinase C delta (PKCδ), inhibited the EoL-1 cell differentiation induced by S100A8 and S100A9. These results suggest that S100A8 and S100A9 may regulate the differentiation of eosinophilic progenitors. Moreover, these findings may shed light on elucidation of eosinophil differentiation due to S100 proteins.
Effect of house dust mite on neutrophil apoptosis by cytokine secretion in lymphocytes
Lee, Na Rae,Lee, Ji-Sook,Baek, Seung Yeop,Kim, Da Hye,Gu, Ayoung,Kim, Seong Yeol,Lee, Soo Jin,Kim, In Sik THE KOREAN SOCIETY OF TOXICOGENOMICS AND TOXICOPRP 2016 MOLECULAR AND CELLULAR TOXICOLOGY Vol. No.
Although extract of Dermatophagoides farinae (DF) alone had no effect on neutrophil apoptosis, it inhibited neutrophil apoptosis in neutrophils cocultured with lymphocytes in both normal and allergic subjects. DF showed a stronger inhibition on the apoptosis of allergic neutrophils cocultured with allergic lymphocytes than that of normal neutrophils cocultured with normal lymphocytes. DF induced the secretion of IL-6, IL-8, MCP-1, and GM-CSF of the normal and allergic lymphocytes. The cytokine secretion due to DF in allergic lymphocytes is higher than in normal lymphocytes. The cytokine secretion of normal and allergic lymphocytes induced by DF was suppressed by PAR2i, a PAR2 inhibitor, LY294002, a PI3K inhibitor, AKTi, an Akt inhibitor, PD98059, an ERK inhibitor, and BAY-11-7085, an <TEX>$NF-{\kappa}B$</TEX> inhibitor. Phosphorylation of ERK induced by DF was suppressed by PAR2i, LY294002 and AKTi, and <TEX>$NF-{\kappa}B$</TEX> activity due to DF was inhibited by PAR2i, LY294002, AKTi, and PD98059.
Seung Yeop Baek,Na Rae Lee,Da Hye Kim,Ayoung Gu,Seong Yeol Kim,Dae-Yong Song,김동희,Hak Joo Choi,Byung-Jun Park,김인식 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.2
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra pars compacta. In this study, we investigated the effects of a novel herb formula, Hepad, on PD. Dose-dependent treatment with 1-methyl-4-phenylpyridinium (MPP+) decreased the viability of SH-SY5Y cells, and Hepad inhibited the toxic effect of MPP+. Hepad blocked the production of reactive oxygen species (ROS) induced by MPP+ in SH-SY5Y cells, and suppressed the activation of caspase 9 and caspase 3 due to MPP+. A rat model of PD was generated by 6-hydroxydopamine (6-OHDA) injection into the left medial forebrain bundle (MFB) of SD rats. In D-amphetamine sulfate-induced rotational behavioral tests, Hepad administration attenuated circling behavior relative to the 6-OHDA-treated disease group. In addition, Hepad treatment significantly increased the tyrosine hydroxylase (TH)-positive cells in the substantia nigra pars compacta (SNpc) that had decreased in response to 6-OHDA treatment (P<0.05). OX-6 expression, which indicates the presence of microglial cells, decreased significantly after treatment of Hepad in contrast to the 6-OHDA-treated disease group (P<0.05). These results indicate that Hepad may be a useful neuroprotective material for the treatment of neurodegenerative disorders such as PD.
In Sik Kim,Mi Ae Im,Na Rae Lee,Seung Yeop Baek,Beom Seok Park,Ayoung Gu,Da Hye Kim,Ji-Sook Lee 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.2
House dust mite is a major allergen in allergic diseases such as asthma. In this study, we investigated the effects of house dust mite on constitutive eosinophil apoptosis in normal and asthmatic subjects. We classified asthmatic subjects into those with atopic and non-atopic asthma depending on the presence of DP-specific IgE or/and DF-specific IgE in serum. Both blood and bronchoalveolar lavage fluid (BALF) eosinophils in atopic asthma were elevated when compared with normal and non-atopic eosinophils. Dermatophagoides pteronissinus extract (DP) inhibited constitutive eosinophil apoptosis of atopic asthmatic subjects, but not that of normal and non-atopic subjects. DF had no effect on eosinophil apoptosis in normal and asthmatic subjects. The anti-apoptotic effects of DP were not altered by E64, a cysteine protease inhibitor, or aprotinin, a serine protease inhibitor, and Der p1 and Der p 2 had no effect on eosinphil apoptosis of normal and asthmatic patients, including atopic and not-atopic patients. Anti-apoptotic signaling mediated by DP in atopic asthma was associated with the TLR4/PI3K/Akt/ERK/NF- κB pathway. Activation of procaspase 3 and procaspase 9 was delayed by DP stimulation. Our results indicate that DP induces eosinophilic inflammation by inhibiting eosinophil apoptosis, and that the inhibitory effect is associated with exposure of asthma subjects to DP. A better understanding of the difference between atopic and non-atopic asthma will help elucidate the pathogenesis and develop methods for treatment of asthma