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Poster Session 2 : Characterization of neural cell types expressing peroxiredoxins in mouse brain
( Mei Hua Jin ),( Young Ho Lee ),( Jin Man Kim ),( Hu Nan Sun ),( Eon Yi Moon ),( Min Ho Shong ),( Sun Uk Kim ),( Sang Ho Lee ),( Tae Hoon Lee ),( Dae Yeul Yu ),( Dong Seok Lee ) 한국생화학분자생물학회 (구 한국생화학회) 2005 생화학분자생물학회 춘계학술발표논문집 Vol.2005 No.-
Tian, Yu-Hua,Lee, Kwang-Wook,You, In-Jee,Lee, Seok-Yong,Jang, Choon-Gon Wiley Subscription Services, Inc., A Wiley Company 2008 Synapse Vol.62 No.8
<P>Butorphanol is a synthetic opioid agonist/antagonist analgesic agent that mainly exerts its effects through κ-opioid receptors. It has been demonstrated that κ-opioid receptors preferentially mediate the development of physical dependence upon butorphanol and the associated withdrawal syndrome. However, it is not fully understood whether or not nNOS-containing neurons in the various brain regions play an important role in butorphanol withdrawal. Therefore, this study was conducted to determine whether the selective nNOS inhibitor, 7-NI, modifies the development of butorphanol withdrawal and changes of nNOS expressions in different brain regions in physically butorphanol-dependent rats. The first part of the study focused on withdrawal behaviors in male Sprague-Dawley rats. Physical dependence was induced by a 72-h i.c.v. infusion with butorphanol (26 nmol/μl/h) and withdrawal was subsequently precipitated by i.c.v. challenge with naloxone (48 nmol/5 μl/rat) 2 h after termination of the butorphanol infusion. The butorphanol/7-NI coadministration group showed a significant decrease in several signs of withdrawal such as teeth chattering, as compared with the butorphanol-treated group. In the second part of the study, immunohistochemical analysis was performed to determine the expression of nNOS in the various brain regions. In the butorphanol/7-NI coadministration group, the number of cells labeled for nNOS was significantly lower in the various brain regions (including the caudate putamen, nucleus accumbens, and hippocampus) than in the butorphanol group. Therefore, 7-NI decreased in butorphanol-induced physical dependence and nNOS expression. Taken together, these findings suggest that the nNOS system is involved in the development of butorphanol-induced physical dependence, and 7-NI has potential clinical application as a candidate for the treatment of opioid withdrawal syndrome. Synapse 62:582–589, 2008. © 2008 Wiley-Liss, Inc.</P>
Kuo-Feng Hua,A-Ching Chao,Ting-Yu Lin,Wan-Tze Chen,Yu-Chieh Lee,Wan-Han Hsu,Sheau-Long Lee,Hsin-Min Wang,Ding-I. Yang,Tz-Chuen Ju 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.4
Background: Huntington's disease (HD) is a neurodegenerative disorder caused by the expansion oftrinucleotide CAG repeat in the Huntingtin (Htt) gene. The major pathogenic pathways underlying HDinvolve the impairment of cellular energy homeostasis and DNA damage in the brain. The protein kinaseataxia-telangiectasia mutated (ATM) is an important regulator of the DNA damage response. ATM isinvolved in the phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK plays acritical role in response to DNA damage. Herein, we demonstrated that expression of polyQ-expandedmutant Htt (mHtt) enhanced the phosphorylation of ATM. Ginsenoside is the main and most effectivecomponent of Panax ginseng. However, the protective effect of a ginsenoside (compound K, CK) in HDremains unclear and warrants further investigation. Methods: This study used the R6/2 transgenic mouse model of HD and performed behavioral tests,survival rate, histological analyses, and immunoblot assays. Results: The systematic administration of CK into R6/2 mice suppressed the activation of ATM/AMPK andreduced neuronal toxicity and mHTT aggregation. Most importantly, CK increased neuronal density andlifespan and improved motor dysfunction in R6/2 mice. Conversely, CK enhanced the expression of Bcl2protected striatal cells from the toxicity induced by the overactivation of mHtt and AMPK. Conclusions: Thus, the oral administration of CK reduced the disease progression and markedlyenhanced lifespan in the transgenic mouse model (R6/2) of HD.
Han Ying-Hao,Mao Ying-Ying,Yu Nan-Nan,Jin Mei-Hua,Jin Ying-Hua,Wang Ai-Guo,Zhang Yong-Qing,Shen Gui-Nan,Cui Yu-Dong,Yu Li-Yun,Lee Dong-Seok,Jo Yu-Jin,Sun Hu-Nan,Kwon Jeongwoo,권태호 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3
In this study, we used RNA sequencing (RNA-seq) to analyze and compare bulk cell samples from wild-type (WT) dermal mesenchymal stem cells (DMSCs) (n = 3) and Prx II knockout DMSCs (n = 3). The purpose of the study was to elucidate the role of Prx II on allogeneic immune rejection of transplanted DMSCs. The results revealed differential expression of 472 genes (176 up-regulated and 296 down-regulated; p ≤ 0.05) between the PrxII+/+ (WT) and PrxII−/− sample groups. When highly regulated genes were categorized according to the Gene Ontology (GO) molecular function classification and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PrxII−/− samples showed a robust downward trend in allograft rejection. The study identified 43 all immunologically rejected differentially expressed genes, of which 41 showed lower expression in the PrxII−/− vs. PrxII+/+ (WT) samples. These findings suggest that Prx II gene knockout may down-regulate the allograft rejection that occurs during DMSCs transplantation and improve the survival rate of DMSCs in the host. This study provides a new perspective on the clinical treatment of stem cell transplantation.
ERTC Involved in HCC Growth and Metastasis through p53 and WNK1 Signaling Pathway
( Hua Li ),( Mi-jin Lee ),( Goung-ran Yu ),( Lan Liu ),( Xue-ji Han ),( Dae-ghon Kim ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: ERTC has been shown to be an important player in the regulation of centrosome/microtubule dynamics during mitosis and found to be deregulated in a variety of human malignancies. But, the functional role and signaling pathway of ERTC in hepatocellular carcinoma (HCC) remains elucidative. Methods: ERTC mRNA and miR-1324 expression was confirmed by real-time PCR analysis in human liver sample. ERTC protein expression was investigated by immunoblotting analysis in HCC cell lines and HCC tissues. The ERTC expression was infected with adenovirus, or knockdown by a delivery with short hairpin RNA (shRNA) or treatment with the potential ERTC inhibitor KHS101 hydrochloride, in Huh7, HepG2, SH-J1 and Alexander cell lines; cells were analyzed for proliferation, migration, and invasion. Tumor metastasis by ERTC and WNK1 was tested in vivo mouse model. Moreover, signaling pathways involved in invasion and metastasis were analyzed by Western blot. Results: ERTC was abundantly expressed in HCC cell lines and HCC tissues compared with non-tumor HCC tissues. ERTC mRNA was positively correlated with the tumor size, worsening differentiation status, lack of fibrous capsule formation, microvessel invasion, intrahepatic metastasis, AFP level and advanced stage of HCC. Knockdown of ERTC in SH-J1 and Alexander cells suppressed migratory and invasive behavior as well as the expression of EMT related markers. Silencing ERTC enhanced p53 expression and decrease phosphorylation of WNK1 in SH-J1 and Alexander cells. The cells with knockdown of ERTC using target shRNA reduced tumor metastasis in a lung metastasis mouse model. Moreover, knockdown of WNK1 also inhibit tumorigenicity and metastatic ability were examined in an orthotopic animal model. miR-1324 interacted with the 3’ untranslated region (3’ UTR) of ERTC. Levels of miR-1324 were correlated inversely with ERTC mRNA and in human HCC samples. Conclusions: Therefore, ERTC may be involved in HCC growth and metastasis through p53 and WNK1 signaling pathway, which may be useful therapeutic targets.
Serial values for hematologic and biochemical analysis after myocardial infarction in rats
Lee, Mi-Jin,Tae, Hyun-Jin,Li, Ying-Hua,Yu, Do-Hyeon,Han, In-Ae,Lee, Seok-Won,Ahn, Dong-Choon,Kim, In-Shik,Park, Jin-Ho The Korean Society of Veterinary Service 2008 韓國家畜衛生學會誌 Vol.31 No.2
To diagnose acute myocardial infarction (MI), many cardiac markers have been used in hematologic and biochemical analysis, and many studies have been published for hematologic and biochemical analysis associated with human acute MI. However, after occurrence of acute MI, the serial investigation for values in hematologic and biochemical analysis including chronic MI has rarely been performed. To observe the change of the serial values in hematologic and biochemical analysis, we induced artificial MI. The left main descending artery (LMDA) of the left coronary artery was ligated during the progression (day 1, 3, 5, 7, 14 and 30) of MI. Total 66 Sprague-Dawley rats were divided into the sham group (n=24, thoracotomy without LMDA ligation) and the experimental (MI) group (n=42, with LMDA ligation). And all individual in each group was sacrified at day 1, 3, 5, 7, 14 and 30 for the hematologic and biochemical analysis. In comparison of hematologic analysis between the sham and MI groups, the mean values of red blood cell (RBCs), hemoglobin and hematocrit (HCT) showed a steady increase. In biochemical analysis, the mean values of glucose, cholesterol, total creatine kinase (CK) and isoenzyme MB, and lactate dehydrogenase (LDH) were increased in all MI groups compared with the sham groups. The results of this study suggest that early hematologic and biochemical mean values occurred after acute MI are similar to those of human acute MI. In conclusion, we could observe the alterations and serial values in hematologic and biochemical analysis to the extent of chronic status after acute MI.