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Lee, Hanbyeol,Park, Jeong-Ran,Kim, Woo Jin,Sundar, Isaac K.,Rahman, Irfan,Park, Sung-Min,Yang, Se-Ran The Federation of American Societies for Experimen 2017 The FASEB Journal Vol.31 No.5
<P>The receptor for advanced glycan end products (RAGE) has been identified as a susceptibility gene for chronic obstructive pulmonary disease (COPD) in genome-wide association studies (GWASs). However, less is known about how RAGE is involved in the pathogenesis of COPD. To determine the molecular mechanism by which RAGE influences COPD in experimental COPD models, we investigated the efficacy of the RAGE-specific antagonist FPS-ZM1 administration in in vivo and in vitro COPD models. We injected elastase intratracheally and the RAGE antagonist FPS-ZM1 in mice, and the infiltrated inflammatory cells and cytokines were assessed by ELISA. Cellular expression of RAGE was determined in protein, serum, and bronchoalveolar lavage fluid of mice and lungs and serum of human donors and patients with COPD. Downstream damage-associated molecular pattern (DAMP) pathway activation in vivo and in vitro and in patients with COPD was assessed by immunofluorescence staining, Western blot analysis, and ELISA. The expression of membrane RAGE in initiating the inflammatory response and of soluble RAGE acting as a decoy were associated with up-regulation of the DAMP-related signaling pathway via Nrf2. FPS-ZM1 administration significantly reversed emphysema in the lung of mice. Moreover, FPS-ZM1 treatment significantly reduced lung inflammation in Nrf2(+/+) , but not in Nrf2(-/-) mice. Thus, our data indicate for the first time that RAGE inhibition has an essential protective role in COPD. Our observation of RAGE inhibition provided novel insight into its potential as a therapeutic target in emphysema/COPD.-Lee, H., Park, J.-R., Kim, W. J., Sundar, I. K., Rahman, I., Park, S.-M., Yang. S.-R. Blockade of RAGE ameliorates elastase-induced emphysema development and progression via RAGE-DAMP signaling.</P>
Differential Expressions of Gap Junction Proteins during Differentiation of Rat Neuronal Stem Cells
Se-Ran Yang,Sung-Dae Cho,Nam-Shik Ahn,Ji-Won Jung,Joon-Suk Park,Nguyen Ba Tiep,Ki-Su Park,In-Sun Hong,Eun-Hye Jo,Min-Su Seo,Byong-Su Yoon,Yong-Soon Lee,Kyung-Sun Kang 한국환경성돌연변이발암원학회 2003 한국환경성돌연변이·발암원학회지 Vol.23 No.1
Gap junctional intercellular communication (GJIC) plays a key role during development, process of tissue differentiation, and in maintenance of adult tissue homeostasis. Neural stem cells leading to formation of cell clusters termed “neurospheres”, can differentiate into neurons, oligodendrocytes, and astrocytes. We investigated the expression levels and distribution of connexin43 (Cx43) and connexin32 (Cx32), abundant gap junctional protein in neural cells and in neurospheres isolated from rat fetus embryonic day (ED) 17. During differentiation of neurospheres, expression of Cx43 and 32 were increased time-dependently within 72 h, and then decreased at 7 day in western blot analysis. TPA-induced inhibition<br/> of GJIC was confirmed by decreased fluorescence by SL/DT assay, and induced hyperphosphorylation of Cx43 while no changes in Cx32 levels in western blot assay. Our results indicate that GJIC may be a crucial role in the differentiation of neuronal stem cell. And this GJIC can be inhibited by TPA through the hyperphosphorylation of Cx43.
Yang, Se-Ran,Kim, Sun-Jung,Byun, Kyoung-Hee,Hutchinson, Brian,Lee, Bong-Hee,Michikawa, Makoto,Lee, Yong-Soon,Kang, Kyung-Sun Wiley (John WileySons) 2006 Stem cells Vol.24 No.2
<P>Neural stem cells (NSCs) are capable of giving rise to neurons, glia, and astrocytes. Although self-renewal and differentiation in NSCs are regulated by many genes, such as Notch and Numb, little is known about the role of defective genes on the self-renewal and differentiation of NSCs from developing brain. The Niemann-Pick type C1 (NPC1) disease is a neurodegenerative disease caused by a mutation of the NPC1 gene that affects the function of the NPC1 protein. The ability of NSC self-renewal and differentiation was investigated using a model of NPC1 disease. The NPC1 disorder significantly affected the self-renewal ability of NSCs, as well as the differentiation. NSCs from NPC1-/- mice showed impaired self-renewal ability compared with the NPC1+/+ mice. These alterations were accompanied by the enhanced activity of p38 mitogen-activated protein kinases (MAPKs). Further, the specific p38 MAPK inhibitor SB202190 improved the self-renewal ability of NSCs from NPC-/- mice. This indicated that the NPC1 deficiency can lead to lack of self-renewal and altered differentiation of NSCs mediated by the activation of p38 MAPK, impairing the generation of neurospheres from NPC1-/- Thus, the NPC1 gene may play a crucial role in NSC self-renewal associated with p38 MAPK.</P>
Study of fibroblast growth factor 2 administration in bleomycin induced pulmonary fibrosis mice
Se Bi Lee,Hyeokku Lee,Jungyu Baek,Eunhyeok Choi,Hyunseung Lee,Juhyeok Hong,Jaehyun Kim,Jeong Yun Park,Gichang Jeong,Jieun Jeon,Jooyeon Lee,Jaehyun Park,Jimin Jang,Sang-Ryul Cha,Se-Ran Yang 한국실험동물학회 2023 한국실험동물학회 학술발표대회 논문집 Vol.2023 No.2
Yang, Se-Ran,Hong, Hee-Do,Cho, Sung-Dae,Ahn, Nam-Shik,Jung, Ji-Won,Park, Joon-Suk,Jo, Eun-Hye,Hwang, Jae-Woong,Sun-bo,Park, Jung-Ran,Lee, Seong-Hun,Jung, Ji-Youn,Choi, Changsun,Kang, Kyung-Sun,Lee, Yo 한국식품위생안전성학회 2005 한국식품위생안전성학회지 Vol.20 No.1
약용식물내 에스트로겐성과 항-에스트로겐성을 조사하고 항암인자를 발견하기 위하여, 본연구는 에탄올추출로 제조된 9종류의 한국산 약용식물에 대하여 재조합효모와 MCF-7 사람유방암세포주를 이용하여 스크리닝하고 비교하였다. 재조합효모를 이용한 실험결과, 7종류의 약용식물에서 에스트로겐성이 나타났고, 4종류에서 안드로겐성이 나타났다. 또한 MCF-7 사람유방암세포주를 이용한 실험결과, 8종류의 추출물이 MCF-7 세포의 성장을 억제하는 것으로 확인되었으며 비스페놀 A와 동시 처치한 경우에도 유의적으로 억제하는 것으로 나타났다. 또한 Clyeyrrhiza uralensis, Cassia tora, Syringa velutina, Zingiber officinale, Malva verticillata, Panax ginseng C.A. Meyer는 식물성 에스트로겐으로서 에스트로겐에 양성인 사람유방암세포의 증식을 유의적으로 억제시티는 흥미로운 결과가 제시되었다. 따라서 이번 연구는 한국산 약용식물이 식물성 에스트로겐과 항암인자로서 이용될 수 있으며, 에스트로겐의 활성을 조사하는데 유용하게 이용될 수 있을 것으로 사료된다. To investigate whether there are estrogenic and anti-estrogenic activities in various medicinal herbs and discover prominent chemo-preventive agents, eye screened and compared the ethanol extracts of 9 plants through the recombinant yeast assay and MCF-7 human breast cancer cell assay. In recombinant yeast assay. seven medicinal herbs showed estrogenicity, and tour extracts showed androgenecity. In MCF-7 proliferation assay. the growth of MCF-7 cells was inhibited by eight extracts before and even alter co-treatment with bisphenol A. It is interesting that the extracts of Glyeyrrhiza uralensis, Cassia tora, Syringa velutina, Zingiber officinale, Malva verticillata, and Ponax ginseng C.A. Meyer exhibited inhibitory effects as phytoestrogens in estrogen-responsive human breast cancer cells. This study suggests that some Korean medicinal herbs might be considered as phytoestrooens and be useful to further analyze those plants which contain the estrogenic effect in order to identify the active principles.
S-389 : 강직성 척추염 환자에서 항 TNF-α치료 후 신증후군의 완전관해와 변화없는 아밀로이드 침착
( Se Yun Kim ),( Eun Young Kim ),( Ju Young Moon ),( Sang Ho Lee ),( Sang Hoon Lee ),( Ran Song ),( Hyung In Yang ),( Sung Jig Lim ) 대한내과학회 2013 대한내과학회 추계학술대회 Vol.2013 No.1
In amyloid A (AA) amyloidosis, tumor necrosis factor (TNF)-α blockers has been reported to be effective in the treatment of both the autoimmune disease and amyloidosis. We describe a case of patient with AA amyloidosis and nephrotic syndrome due to underlying ankylosing spondylitis who was effectively treated with an etanercept. In the second kidney biopsy, there were little changes in the degree of amyloid deposition, however, the interstitial inflammation and foot process effacement were fully recovered. These findings suggest the local inflammatory process in the kidney is important in development of proteinuria in amyloidosis.
Simple and Novel Assay of the Host-Guest Complexation of Homocysteine with Cucurbit[7]uril
( Se-ho Park ),( Jae-yeul Lee ),( Hyun-nam Cho ),( Kyoung-ran Kim ),( Seun-ah Yang ),( Hee-joon Kim ),( Kwang-hwan Jhee ) 한국미생물 · 생명공학회 2019 Journal of microbiology and biotechnology Vol.29 No.1
This paper introduces three ways to determine host-guest complexation of cucurbit[7]uril (CB[7]) with homocysteine (Hcy). After preincubating Hcy and cysteine (Cys) with CB[7], Ellman’s reagent (DTNB) was used to detect Hcy and Cys. Only Cys reacted with DTNB and Hcy gave a retarded color change. This suggests that the -SH group of Hcy is buried inside CB[7]. Human cystathionine γ-lyase (hCGL) decreased the level of Hcy degradation after preincubating Hcy and CB[7]. These results suggest that the amount of free Hcy available was decreased by the formation of a Hcy-CB[7] complex. The immunological signal of anti-Hcy monoclonal antibody was decreased significantly by preincubating CB[7] with Hcy. The ELISA results also show that ethanethiol group (-CH2CH2SH) of Hcy, which is an epitope of anti-Hcy monoclonal antibody, was blocked by the cavity in CB[7]. Overall, CB[7] can act as a host by binding selectively with Hcy, but not Cys. The calculated half-complexation formation concentration of CB[7] was 58.2 nmol using Ellman’s protocol, 97.9 nmol using hCGL assay and 87.7 nmol using monoclonal antibody. The differing binding abilities of Hcy and Cys towards the CB[7] host may offer a simple and useful method for determining the Hcy concentration in plasma or serum.
Differential Expressions of Gap Junction Proteins during Differentiation of Rat Neuronal Stem Cells
Yang, Se-Ran,Cho, Sung-Dae,Ahn, Nam-Shik,Jung, Ji-Won,Park, Joon-Suk,Tiep, Nguyen Ba,Park, Ki-Su,Hong, In-Sun,Jo, Eun-Hye,Seo, Min-Seo,Yoon, Byong-Su,Lee, Yong-Soon,Kang, Kyung-Sun Korean Environmental Mutagen Society 2003 한국환경성돌연변이·발암원학회지 Vol.23 No.1
Gap junctional intercellular communication (GJIC) plays a key role during development, process of tissue differentiation, and in maintenance of adult tissue homeostasis. Neural stem cells leading to formation of cell clusters termed 'neurospheres', can differentiate into neurons, oligodendrocytes, and astrocytes. We investigated the expression levels and distribution of connexin43 (Cx43) and connexin32 (Cx32), abundant gap junctional protein in neural cells and in neurospheres isolated from rat fetus embryonic day (ED) 17. During differentiation of neurospheres, expression of Cx43 and 32 were increased time-dependently within 72 h, and then decreased at 7 day in western blot analysis. TPA-induced inhibition of GJIC was confirmed by decreased fluorescence by SL/DT assay, and induced hyperphosphorylation of Cx43 while no changes in Cx32 levels in western blot assay. Our results indicate that GJIC may be a crucial role in the differentiation of neuronal stem cell. And this GJIC can be inhibited by TPA through the hyperphosphorylation of Cx43.
Se-Ran Yang,Soojin Jang,Jooyeon Lee,Se Min Ryu,Hanbyeol Lee,Jeong-Ran Park,Aera Jang,Dongwook Kim,Hyejin Kim 한국예방수의학회(구 한국수의공중보건학회) 2017 예방수의학회지 Vol.42 No.2
Colorectal cancer is a major cause of morbidity and mortality that accounts for over 9% of all incidences of cancer. Additionally, colorectal cancer is widely recognized as an environmental disease related to ill-defined cultural, social and lifestyle factors including physical activity, obesity, cigarette smoking and heavy alcohol consumption. Accordingly, natural phytochemicals and extracts have attracted attention because of their beneficial biological effects. Coenzyme Q10 (CoQ10) is a common supplementary medicine applied to increase bioenergetic capacity in various diseases. Therefore, in this study, we investigated whether CoQ10 treatment has any inhibitory effects and its related cellular mechanisms in human colon cancer HCT116 cells. A MTT assay revealed that CoQ10 slightly decreased the proliferation of HCT116 cells; however, glutathione- and superoxide dismutase- activity were unchanged in response to CoQ10 treatment. A DCF-DA assay revealed that CoQ10 slightly increased ROS release of HCT116 cells. However, in a nitric oxide (NO) assay, CoQ10 significantly increased NO production in a dose-dependent manner. The results of western blot analysis revealed that the protein levels of Bax, p21 and p53 were increased, whereas the protein level of Bcl2 was decreased suggesting that the CoQ10-mediated inhibitory mechanism is associated with apoptotic signaling. Taken together, our findings indicate that CoQ10 has an inhibitory effect on the growth of colon cancer cells via NO production that is associated with regulation of factors involved in apoptotic signaling including Bax, Bcl2, p21 and p53.