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정시정 ( Jeong Si Jeong ),김청수 ( Kim Cheong Su ),장재원 ( Jang Jae Won ),김순배 ( Kim Sun Bae ),이상구 ( Lee Sang Gu ),박정식 ( Park Jeong Sig ) 대한신장학회 2003 Kidney Research and Clinical Practice Vol.22 No.3
배 경 : Monocyte chmoattractant protein-1 (MCP-1)과 reactive oxygen species (ROS)는 사구체 손상의 유발 및 진행에 중요한 역할을 담당하는 것으로 알려져 있다. 연구자들은 사람의 메산지움세포에서 pro-inflammatory cytokine에 의한 MCP-1 발현 및 lysophosphatidylcholine에 의한 세포 내 ROS 형성에 아스피린의 체내 대사산물인 salicylate가 미치는 영향을 알아보고자 하였다. 방 법 : 메산지움세포를 salicylate로 전처리 한 후 tumor necrosis factor-α(TNF-α)와 interleukin-1β(IL-1β)로 자극하여 salicylate가 MCP-1 발현 및 nuclear factor-κB (NF-κB)에 미치는 영향을 알아보았다. MCP-1 mRNA와 단백의 발현 정도는 각각 Northern blot analysis와 효소면역측정법을 이용하여 측정하였고 NF-κB의 활성도 및 NF-κB 억제 단백인 IκB-α의 발현은 각각 electrophoretic mobility shift assay와 Western blot analysis를 이용하여 측정하였다. Lysophosphatidylcholine에 의한 세포 내 ROS의 형성은 2`7`-dichlorofluorescein diacetate를 이용하여 flow cytometry로 측정하였다. 결 과 : Salicylate는 TNF-α와 IL-1β에 의한 MCP-1 mRNA 및 MCP-1 단백 발현을 농도에 비례하여 (1-20 mM) 억제하였으며 이런 억제 효과는 cycloheximide에 의해 영향을 받지 않았다. 또한 salicylate TNF-α와 IL-1β에 의한 NF-κB의 활성화를 농도에 비례하여 (1-20 mM) 억제하였으며 TNF-α에 의한 IκB-α단백의 분해도 억제하였다. 1 mM 이하의 저 농도 salicylate (0.05-1 mM)도 lysophosphatidylcholine에 의한 세포 내 ROS의 생성을 억제 하였다. 결 론 : Salicylate는 사람의 메산지움세포에서 TNF-α와 IL-1β에 의한 MCP-1 mRNA 및 단백 발현을 억제하였으며 이러한 효과는 적어도 일부는 IκB-α단백의 분해 억제 따른 NF-κB의 활성화 억제에 기인하였다. 그러나 이런 효과를 나타내기 위해서는 1 mM 이상의 고농도의 salicylate가 필요하였다. 반면 lysophosphatidylcholine에 의한 세포 내 ROS 생성 억제 효과는 1 mM 이하의 저농도에서도 관찰할 수 있었다. Background: Monocyte chemoattractant protein-1 (MCP-1) and reactive oxygen species (ROS) play an important role during glomerular inflammation. We investigated the effect of aspirin metabolite, salicylate on the pro-inflammatory cytokine-induced MCP-1 expression and lysophosphatidylcholine -induced in-tracellular ROS formation in human mesangial cells. Methods: Cells were pretreated with salicylate, and then timulated with tumor necrosis factor-α (TNF-α) or interleukin-1β (IL-1β). The expression of MCP-1 mRNA and MCP-1 protein were measured by Northern blot analysis and enzyme-linked immunosorbent assay, respectively. Nuclear factor-κB (NF-κB) activity was measured by electrophoretic mobility shift assay. Degradation of IκB-α was assessed by Western blot analysis. Intracellular ROS production was monitored by flow cytometry using 2`7`-dichlorofluorescin diacetate. Results: Salicylate inhibited the TNF-α- or IL-1β induced MCP-1 mRNA expression in a dose dependent manner (1-20 mM) and also suppressed the MCP-1 protein expression. Its effect was not attributable to de novo synthesis of intermediary proteins. Salicylate inhibited the TMF-α- of IL-1β-induced NF-κB binding activity and also suppressed the TNF-α-induced IκB-α degradation. Low concentration of salicylate (0.01-1 mM) suppressed the lysophosphatidylcholine-induced ROS formation. Conclusion: Milimolar concentration of salicylate inhibited the MCP-1 expression at least in part, via suppression of NF-κB by reducing the degradation of IκB-α. On the other hand, lower concentration of salicylate could suppress th lysophosphatidylcho-line-induced intracellular ROS formation. (Krean J Nephrol 2003;22(3):261-272)
하정식 ( Ha Jeong Sig ),정인배 ( Jeong In Bae ),조주형 ( Jo Ju Hyeong ),이향아 ( Lee Hyang A ),엄민섭 ( Eom Min Seob ),박광화 ( Park Gwang Hwa ) 대한산부인과학회 2003 Obstetrics & Gynecology Science Vol.46 No.11
Intramural pregnancy is one of the rarest forms of ectopic pregnancy. The pathologic diagnosis of the intramural ectopic pregnancy requires that the myometrium surrounds the products of conception separated from the endometrial cavity or fallopian tubes.
Preliminary Design of GBAS Onboard Test Equipment
Jeong, Myeong-Sook,Ko, Wan-Jin,Bae, Joong Won,Jun, Hyang Sig The Institute of Positioning 2013 Journal of Positioning, Navigation, and Timing Vol.2 No.1
When the ground subsystem of Ground Based Augmentation System(GBAS) is installed at the airport, the functions and performance of subsystem should be evaluated through ground and flight testing at the pre-commissioning phase. In the case of GBAS flight testing, it can be conducted by the existing flight check aircraft, but the GBAS ground testing requires the development of specially customized equipment to perform the ground testing. Therefore, this paper describes the preliminary design of GBAS onboard test equipment which can be independently used for the GBAS ground testing and flight testing on a car and an aircraft.
Dequalinium-based functional nanosomes show increased mitochondria targeting and anticancer effect
Bae, Yoonhee,Jung, Min Kyo,Lee, Seulgi,Song, Su Jeong,Mun, Ji Young,Green, Eric S.,Han, Jin,Ko, Kyung Soo,Choi, Joon Sig WISSENSCHAFTLISCHE VERLAGSGESELLSCHAFT MBH 2018 EUROPEAN JOURNAL OF PHARMACEUTICS AND BIOPHARMACEU Vol.124 No.-
<P><B>Abstract</B></P> <P>Mitochondria are targets with great potential for therapeutics for many human disorders. However, drug delivery systems for such therapeutics remain in need of more efficient mitochondrial-targeting carriers. In this study, we report that nanosomes composed of Dequalinium/DOTAP (1,2-dioleoyl-3-trimethylammonium-propane)/DOPE (1,2-dioleoyl-<I>sn</I>-glycero-3-phosphoethanolamine), called DQA80s, can act in the dual role of mitochondrial-targeting carrier and anticancer agent for therapeutic interventions against mitochondrial diseases. In cytotoxicity assays, DQA80s were shown to be more toxic than DQAsomes. The DQA80s showed significantly increased cellular uptake as compared to that of DQAsomes, and DQA80s also showed more efficient escape from the endolysosome to the cytosol. We observed the efficient targeting of DQA80s to mitochondria in living cells using flow cytometry, confocal microscopy, and TEM imaging. We also found evidence of anticancer potential that mitochondrial-targeted DQA80s induced apoptosis by production of reactive oxygen species (ROS) via MAPK signaling pathways, loss of mitochondrial membrane potential, and the caspase-3 activation. The present study demonstrates that DQA80s have excellent dual potential both as a carrier and as an anticancer therapeutic for mitochondria-related disease therapy <I>in vivo</I>.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Functional nanosome for enhanced mitochondria-targeted gene delivery and expression
Bae, Yoonhee,Jung, Min Kyo,Song, Su Jeong,Green, Eric S.,Lee, Seulgi,Park, Hyun-Sook,Jeong, Seung Hun,Han, Jin,Mun, Ji Young,Ko, Kyung Soo,Choi, Joon Sig Elsevier 2017 Mitochondrion Vol.37 No.-
<P><B>Abstract</B></P> <P>Mitochondria dysfunction plays a role in many human diseases. Therapeutic techniques for these disorders require novel delivery systems that can specifically target and penetrate mitochondria. In this study, we report a novel nanosome composed of dequalinium-DOTAP-DOPE (1,2 dioleoyl-3-trimethylammonium-propane-1,2-dioleoyl-<I>sn</I>-glycero-3-phosphoethanolamine) (DQA80s) as a potential mitochondria-targeting delivery vector. The functional DQAsome, DQA80s, showed enhanced transfection efficiency compared to a vector DQAsomes in HeLa cells and dermal fibroblasts. In addition, DQA80s/pDNA complexes exhibited rapid escape from the endosome into the cytosol. We observed the delivery of pDNA to mitochondria in living cells using flow cytometry, confocal microscopy, and TME imaging. More specifically, we confirmed our results by co-localization of hmtZsGreen constructs to mitochondria when delivered via DQAsomes and DQA80s in living cells. The mitochondria-targeting DQAsomes and DQA80s induced mitochondrial dysfunction through depolarization of mitochondrial membrane potential. Our data demonstrate that DQA80s show promise for use as a mitochondria-targeted carrier system for treatment of mitochondria diseases in vivo.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Formulation and characterization of novel nanosome as a potential mitochondria-targeting delivery vector </LI> <LI> DQA80s/pDNA complexes exhibited a rapid endolysosomal escape and enhanced mitochondrial targeting in living cells. </LI> <LI> DQA80s/hmtGFP construct complexes showed expression at mitochondrial region in living cells. </LI> <LI> DQA80s induced mitochondria dysfunction via depolarization of mitochondrial membrane potential in cancer cells. </LI> </UL> </P>
Bae, Yoonhee,Green, Eric S.,Kim, Goo-Young,Song, Su Jeong,Mun, Ji Young,Lee, Sunray,Park, Jong-Il,Park, Jong-sang,Ko, Kyung Soo,Han, Jin,Choi, Joon Sig Elsevier 2016 International journal of pharmaceutics Vol.515 No.1
<P><B>Abstract</B></P> <P>Glioblastoma multiform (GBM) is the most frequent and aggressive form of brain tumors in adults. However, the development of more efficient and safe nonviral vector gene therapy represents a promising therapeutic approach, using a tumor-specific killer gene, named apoptin. In this study, we describe the efficacy of non-viral gene delivery vectors, the amino acid-conjugated PAMAM derivatives (PAMAM-H-R and PAMAM-H-K) in delivering a therapeutic gene, displaying affinity toward human primary glioma cells (GBL-14 cells) and dermal fibroblasts. We analyzed transfection efficiency, using luciferase (Luci) and a pDNA encoding for enhanced fluorescent protein (EGFP), and cytotoxicity in both cells. The results show that transfection efficiency of PAMAM-H-R improved compared to native PAMAM dendrimer, but cytotoxicity of PAMAM-H-R and PAMAM-H-K were very low. We treated both cells with a polyplex formation of PAMAM-H-R or PAMAM-H-K/apoptin, and analyzed their cellular uptake and localization by flow cytometry and confocal microscopy. Furthermore, we analyzed the endosomal escape effect using TEM images, and found that PAMAM-H-R showed very fast escape from endosome to the cytosol. Caspase 3 activity assay, cell cycle distribution, and JC-1 analysis showed apoptosis induced by apoptin in GBL-14 cells. This indicates that PAMAM-H-R can be a potential nonviral vector gene delivery carrier for brain tumor therapy. The present study demonstrates that PAMAM-H-R/apoptin gene polyplex can be used as an effective therapeutic candidate for GBM due to its selective induction of apoptosis in primary glioma cells as a potential nonviral gene delivery carrier for brain tumor therapy.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
자궁내막암 세포주 Hec-1A에서 sorafenib과 celecoxib에 의한 세포증식억제와 혈관내피성장인자의 발현 변화
김정식 ( Jeong Sig Kim ),박보라 ( Bo Ra Park ),남계현 ( Gye Hyun Nam ),배동한 ( Dong Han Bae ) 대한산부인과학회 2012 Obstetrics & Gynecology Science Vol.55 No.11
목적 자궁내막암 세포주 Hec-1A에서 sorafenib과 celecoxib에 의한 세포증식억제 및 혈관내피성장인자(vascular endothelial growth factor, VEGF)의 발현 변화에 대해 연구하고자 하였다. 연구방법 Hec-1A 세포주에 대한 sorafenib과 celecoxib의 처치 농도와 시간에 따른 세포증식억제 작용을 (3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H-tetrazolium, inner salt) assay로 측정하였으며, 또한 위 약제들을 단독 또는 병합투여시 VEGF, p53의 변화를 역전사-중합효소연쇄반응(reverse transcription-polymerase chain reaction)으로 측정하였다. 결과 Sorafenib과 celecoxib 각각을 자궁내막암 세포주인 Hec-1A에 처치 시, sorafenib의 농도를 5 ng/mL, 10 ng/mL, 20 ng/mL, 50 ng/mL로 증가시킬수록 모든 농도에서 의미 있게 점차적으로 세포들의 증식이 억제되었으며, celecoxib는 60 μmol/L의 농도에서부터 통계적으로 유의하게 차이가 났다. Sorafenib 10 ng/mL을 단독 처리하였을 때보다 celecoxib를 병합처리하였을 때 약제 간 상승 작용으로 세포증식억제의 차이가 통계적으로 의미 있게 나타났다(P<0.0001). 혈관신생과 관련된 VEGF는 sorafenib과 celecoxib 두 가지 약제를 동시에 병합시 sorafenib 단독 처치보다 발현감소가 의미 있게 나타났다. 그러나 p53의 경우 sorafenib이나 celecoxib를 각각 또는 병합처리하며 시간과 농도를 다르게 하여도 약제들에 따른 발현의 변화는 나타나지 않았다. 결론 본 연구결과로 sorafenib과 celecoxib의 병합처치에 의해 Hec-1A자궁내막암 세포주의 증식과 VEGF의 발현이 억제되므로, 자궁내막암의 기존 치료요법에 위 약제들이 보조적인 역할을 할 수 있으리라 생각된다. Objective The aim of this study was to investigate whether combination of sorafenib and celecoxib exhibited an anti-tumor efficacy or altered expression of vascular endothelial growth factor (VEGF) in Hec-1A endometrial cancer cell line. Methods To determine whether sorafenib or celecoxib-induced growth inhibition was determined by the (3-[4,5-dimethylthiazol-2-yl]-5-[3- carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H-tetrazolium, inner salt) assay. Expression of VEGF and p53 were evaluated using the reverse transcription polymerase chain reaction. Results Combination of sorafenib 10 ng/mL and celecoxib 50 μmol/L exhibited synergistic inhibitory effects compared to treatment with each agent alone (P <0.0001). VEGF expression was also down regulated after 24 hours or 72 hours of treatment with sorafenib alone or in combination with sorafenib and celecoxib in Hec-1A cells. However, there was no alteration of p53 expression in Hec- 1A cells after 24 hours or 72 hours of treatment with sorafenib alone or in combination with sorafenib and celecoxib. Conclusion Combination treatment of sorafenib and celecoxib to Hec-1A endometrial cancer cell line revealed the ability to inhibit growth and expression of VEGF.
Distribution of Micronutrients in Plastic Film House Soils of Yeongnam Province
Jong-Bae Chung(정종배),Bok-Jin Kim(김복진),Kwan-Sig Ryu(유관식),Seung-Ho Lee(이승호),Hyun-Jin Shin(신현진),Tae-Kyung Hwang(황태경),Hee-Youl Choi(최희열),Yong-Woo Lee(이용우),Yoon-Jeong Lee(이윤정),Jong-Jib Kim(김종집) 한국토양비료학회 2006 한국토양비료학회지 Vol.39 No.4
대한간학회지 제8차 춘계학술대회 초록집 : 구연 ; 간이식 후 B형 간염 재발방지를 위한 저용량 헤파빅 근주 및 라미부딘 병용효과
배시현 ( Bae Si Hyeon ),조세현 ( Jo Se Hyeon ),윤승규 ( Yun Seung Gyu ),양진모 ( Yang Jin Mo ),한준열 ( Han Jun Yeol ),이창돈 ( Lee Chang Don ),차상복 ( Cha Sang Bog ),정규원 ( Jeong Gyu Won ),선희식 ( Seon Hui Sig ),박두호 ( Park 대한간학회 2002 Clinical and Molecular Hepatology(대한간학회지) Vol.8 No.2(S)