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Lee, Dong-Youb,Won, Kyung-Jong,Lee, Kang Pa,Jung, Seung Hyo,Baek, Suji,Chung, Hyun Woo,Choi, Wahn Soo,Lee, Hwan Myung,Lee, Byeong Han,Jeon, Byeong Hwa,Kim, Bokyung Elsevier 2018 Toxicology and applied pharmacology Vol.347 No.-
<P><B>Abstract</B></P> <P>Angiotensin II (Ang II) is implicated in the development of cardiovascular disorders including hypertension and atherosclerosis. However, the role of Ang II in the interaction between apurinic/apyrimidinic endonuclease/redox factor-1 (APE/Ref-1) and sphingosine-1-phosphate (S1P) signals in relation to vascular disorders remains to be clarified. This study aimed to determine whether APE/Ref-1 plays a role in epigenetic regulation of the S1P receptor (S1PR) in response to Ang II in vascular smooth muscle cell (VSMC) migration and vascular neointima formation. Ang II augmented the expression of S1PR1 in aortic smooth muscle cells of Sprague Dawley rats (RASMCs), which was attenuated by Ang II receptor (AT) 1 inhibitors, antioxidants, and APE/Ref-1 knockdown with small interference RNA. Ang II stimulation produced H<SUB>2</SUB>O<SUB>2</SUB>, and exogenous H<SUB>2</SUB>O<SUB>2</SUB> elevated S1PR1 expression in RASMCs. Moreover, Ang II caused translocation of cytoplasmic APE/Ref-1 into the nucleus in RASMCs. H3 histone acetylation and APE/Ref-1 binding at the S1PR1 promoter were increased in RASMCs treated with Ang II. In addition, Ang II induced migration in RASMCs, which was suppressed by AT1 and S1PR1 inhibitors. The expression of S1PR1, and colocalization of APE/Ref-1 and acetylated histone H3 in vascular neointima, were greater in Ang II-infused rats compared with a control group. These findings demonstrate that Ang II stimulates the epigenetic regulation of S1PR1 expression via H<SUB>2</SUB>O<SUB>2</SUB>-mediated APE/Ref-1 translocation, which may consequently be involved in Ang II-induced VSMC migration and vascular neointima formation. Therefore, APE/Ref-1-mediated overexpression of S1PR1 may be implicated in the vascular dysfunction evoked by Ang II.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ang II increased S1PR1 expression and H<SUB>2</SUB>O<SUB>2</SUB> generation in VSMCs. </LI> <LI> H<SUB>2</SUB>O<SUB>2</SUB> elevated S1PR1 expression in VSMCs. </LI> <LI> Ang II epigenetically enhanced S1PR1 expression via APE/Ref-1 translocation by H<SUB>2</SUB>O<SUB>2</SUB>. </LI> <LI> These events may be linked to Ang II-increased VSMC migration and vascular neointima. </LI> </UL> </P>
Lee, Lim-Kyu,Kim, Ju-Hyun,Kim, Mee-Young,Lee, Jeong-Uk,Yang, Seung-Min,Jeon, Hye-Joo,Lee, Won-Deok,Noh, Ji-Woong,Kwak, Taek-Yong,Jang, Sung-Ho,Lee, Tae-Hyun,Kim, Bokyung,Kim, Junghwan The Society of Physical Therapy Science 2014 JOURNAL OF PHYSICAL THERAPY SCIENCE Vol.26 No.5
<P> [Purpose] An understanding of pain is very important in the study of nanophysiotherapy. In this review, we summarize the mechanisms of endothelin-1 (ET-1)- and mitogen-activated protein kinase (MAPK)-related pain, and suggest their applications in pain physiotherapy. [Method] This review focuses on the signal transduction of pain and its mechanisms. [Results] Our reviews show that mechanisms of ET-1- and MAPK-related pain exist. [Conclusions] In this review article, we carefully discuss the signal transduction in ET-1- and MAPK-related pain with reference to pain nanophysiotherapy from the perspective of nanoparticle-associated signal transduction.</P>
Kim, Bokyung,Kim, Yeon Soo,Ahn, Hye-Mi,Lee, Hyo Jin,Jung, Min Kyu,Jeong, Hyun Yong,Choi, Dong Kyu,Lee, Jun Hyeog,Lee, Sang-Rae,Kim, Jin Man,Lee, Dong-Seok Spandidos Publications 2017 International journal of oncology Vol.51 No.1
<P>Gastric cancer is one of the leading causes of cancer related deaths worldwide. Despite the advanced surgical resection techniques and anticancer drugs currently available to treat early stage gastric cancer, the prognosis of patients with gastric cancer remains poor. The epithelial to mesenchymal transition (EMT) is an important process for the initiation of tumorigenesis. Recent studies suggested that reactive oxygen species (ROS) can promote cell migration and invasion. Thus, an imbalance of redox homeostasis can result in cancer cells exhibiting EMT properties. PRXs are upregulated in various tumors in the breast, bladder, lung, cervical, ovarian, prostate, esophageal, and hepatocellular. However, PRX expression and its impact on disease prognosis, patient survival rate, and EMT are rarely studied in the context of human gastric cancer. The expression of PRX5 was significantly correlated with tumor size, depth of tumor, lymphatic invasion in patients of gastric cancer. In addition, overexpression of PRX5 enhanced carcinogenicity by increasing the proliferation and invasiveness of gastric cancer cells via upregulation of Snail. Taken together, we suggest that PRX5 may be a potential factor that may contribute to poor prognosis of gastric cancer through enhancing the mesenchymal phenotype. Finally, PRX5 is a putative therapeutic target and clinical strategy for various cancers overexpressing PRX5.</P>
MinSoo Byun,Dahyun Yi,JunHo Lee,YoungMin Choe,BoKyung Sohn,JunYoung Lee,HyoJung Choi,Hyewon Baek,YuKyeong Kim,YunSang Lee,ChulHo Sohn,Inhee MookJung,Murim Choi,YuJin Lee,DongWoo Lee,SeungHo Ryu,ShinGy 대한신경정신의학회 2017 PSYCHIATRY INVESTIGATION Vol.14 No.6
Objective-The Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s disease (KBASE) aimed to recruit 650 individuals, aged from 20 to 90 years, to search for new biomarkers of Alzheimer’s disease (AD) and to investigate how multi-faceted lifetime experiences and bodily changes contribute to the brain changes or brain pathologies related to the AD process. Methods-All participants received comprehensive clinical and neuropsychological evaluations, multi-modal brain imaging, including magnetic resonance imaging, magnetic resonance angiography, [11C]Pittsburgh compound B-positron emission tomography (PET), and [18F]fluorodeoxyglucose-PET, blood and genetic marker analyses at baseline, and a subset of participants underwent actigraph monitoring and completed a sleep diary. Participants are to be followed annually with clinical and neuropsychological assessments, and biannually with the full KBASE assessment, including neuroimaging and laboratory tests. Results-As of March 2017, in total, 758 individuals had volunteered for this study. Among them, in total, 591 participants-291 cognitively normal (CN) old-aged individuals, 74 CN young- and middle-aged individuals, 139 individuals with mild cognitive impairment (MCI), and 87 individuals with AD dementia (ADD)-were enrolled at baseline, after excluding 162 individuals. A subset of participants (n=275) underwent actigraph monitoring. Conclusion-The KBASE cohort is a prospective, longitudinal cohort study that recruited participants with a wide age range and a wide distribution of cognitive status (CN, MCI, and ADD) and it has several strengths in its design and methodologies. Details of the recruitment, study methodology, and baseline sample characteristics are described in this paper.
Lee, Hwan Myung,Jeon, Byeong Hwa,Won, Kyung-Jong,Lee, Chang-Kwon,Park, Tae-Kyu,Choi, Wahn Soo,Bae, Young Min,Kim, Hyo Shin,Lee, Sang Ki,Park, Seung Hwa,Irani, Kaikobad,Kim, Bokyung Ovid Technologies Wolters Kluwer -American Heart A 2009 Circulation research Vol.104 No.2
<P>The role of apurinic/apyrimidinic endonuclease-1/redox factor-1 (Ref-1) in vascular smooth muscle cells has yet to be clearly elucidated. Therefore, we attempted to determine the roles of Ref-1 in the migration induced by platelet-derived growth factor (PDGF)-BB and in its signaling in rat aortic smooth muscle cells (RASMCs). Cellular migration, superoxide (O(2)(-*)) production, Rac-1 activity, and neointima formation were determined in cells transfected with adenoviruses encoding for Ref-1 (AdRef-1) and small interference RNA of Ref-1. Overexpression of Ref-1 induced by treatment with RASMCs coupled with AdRef-1 inhibited the migration induced by PDGF-BB. PDGF-BB also increased the phosphorylation of the PDGFbeta receptor, spleen tyrosine kinase (Syk), mitogen-activated protein kinase, and heat shock protein 27, but these increases were significantly inhibited by AdRef-1 treatment. PDGF-BB increased O(2)(-*) production and Rac-1 activity, and these were diminished in cells transfected with AdRef-1. In contrast, RASMC migration, phosphorylation of Syk and O(2)(-*) production in response to PDGF-BB were increased by the knock down of Ref-1 with small interference RNA. The phosphorylation of PDGFbeta receptor in response to PDGF-BB was inhibited completely by the Syk inhibitor and was partly attenuated by a NADPH oxidase inhibitor. PDGF-BB increased the sprout outgrowth of the aortic ring ex vivo, which was inhibited in the AdRef-1-infected RASMCs as compared with the controls. Balloon injury-induced neointimal formation was significantly attenuated by the gene transfer of AdRef-1. These results indicate that Ref-1 inhibits the PDGF-mediated migration signal via the inhibition of reactive oxygen species-mediated Syk activity in RASMCs.</P>
Diminished expression of dihydropteridine reductase is a potent biomarker for hypertensive vessels
Lee, Chang-Kwon,Han, Jin Soo,Won, Kyung-Jong,Jung, Seung-Hyo,Park, Hyo-Jun,Lee, Hwan Myung,Kim, Junghwan,Park, Young Shik,Kim, Hyun-Jung,Park, Pyo-Jam,Park, Tae-Kyu,Kim, Bokyung WILEY-VCH Verlag 2009 Proteomics Vol.9 No.21
<P>To identify the new targets for hypertension, we analyzed the protein expression profiles of aortic smooth muscle in spontaneously hypertensive rats (SHR) of various ages during the development of hypertension, as well as in age-matched normotensive Wistar–Kyoto (WKY) rats, using a proteomic analysis. The expressions of seven proteins were altered in SHR compared with WKY rats. Of these proteins, NADH dehydrogenase 1α, GSTω1, peroxi-redoxin I and transgelin were upregulated in SHR compared with WKY rats. On the other hand, the expression of HSP27 and Ran protein decreased in SHR. The diminution of dihydrobiopterin reductase, an enzyme located in the regeneration pathways of tetrahydrobiopterin (BH4), was also prominent in SHR. The results from a PCR analysis revealed that the expression of BH4 biosynthesis enzymes – GTP cyclohydrolase-1 and sepiapterin reductase – decreased and increased, respectively, in SHR compared with WKY rats. The level of BH4 was less in aortic strips from SHR than from WKY rats. Moreover, treatment with BH4 inhibited aortic smooth muscle contraction induced by serotonin. These results suggest that the deficiency in BH4 regeneration produced by diminished dihydrobiopterin reductase expression is involved in vascular disorders in hypertensive rats.</P>
Lee, Chang-Kwon,Park, Hyo-Jun,So, Hyeon Ha,Kim, Hyo Jin,Lee, Keun Sang,Choi, Wahn Soo,Lee, Hwan Myung,Won, Kyung-Jong,Yoon, Taek Joon,Park, Tae-Kyu,Kim, Bokyung WILEY-VCH Verlag 2006 Proteomics Vol.6 No.24
<P>We used 2-DE and MALDI-TOF/TOF to identify proteins of vascular smooth muscle cells whose expression was or was not altered by exposure to 500 μM H<SUB>2</SUB>O<SUB>2</SUB> for 30 min. We detected more than 800 proteins on silver-stained gels of whole protein extracts from rat aortic smooth muscle strips. Of these proteins, 135 clearly unaffected and 19 having levels altered by exposure to H<SUB>2</SUB>O<SUB>2</SUB> were identified. Protein characterization revealed that the most prominent vascular smooth muscle proteins were those with antioxidant, cytoskeletal structure, or muscle contraction. In addition, cofilin, an isoform of the actin depolymerizing factor family, shifted to its basic site on the 2-DE gel as a result of H<SUB>2</SUB>O<SUB>2</SUB> treatment. In Western blot analysis of proteins from A7r5 aortic smooth muscle cells, the phosphorylation, but not the expression, of cofilin was decreased by H<SUB>2</SUB>O<SUB>2</SUB> in a dose-dependent manner. The H<SUB>2</SUB>O<SUB>2</SUB>-induced dephosphorylation of cofilin and apoptosis was inhibited by Na<SUB>3</SUB>VO<SUB>4</SUB>, an inhibitor of protein tyrosine phosphatase (PTP). These results suggest that cofilin is one of the proteins regulated by H<SUB>2</SUB>O<SUB>2</SUB> treatment in vascular smooth muscle, and has an important role in the induction of vascular apoptosis through PTP-dependent mechanisms.</P>
Lee, Young Mook,Park, Seong H,Shin, Dong-Ik,Hwang, Jee-Yeon,Park, Bokyung,Park, Yun-Jong,Lee, Tae H,Chae, Ho Z,Jin, Byung K,Oh, Tae H,Oh, Young J American Society for Biochemistry and Molecular Bi 2008 The Journal of biological chemistry Vol.283 No.15
<P>The aim of this study was to investigate changes in protein profiles during the early phase of dopaminergic neuronal death using two-dimensional gel electrophoresis in conjunction with mass spectrometry. Several protein spots were identified whose expression was significantly altered following treatment of MN9D dopaminergic neuronal cells with 6-hydroxydopamine (6-OHDA). In particular, we detected oxidative modification of thioredoxin-dependent peroxidases (peroxiredoxins; PRX) in treated MN9D cells. Oxidative modification of PRX induced by 6-OHDA was blocked in the presence of N-acetylcysteine, suggesting that reactive oxygen species (ROS) generated by 6-OHDA induce oxidation of PRX. These findings were confirmed in primary cultures of mesencephalic neurons and in rat brain injected stereotaxically. Overexpression of PRX1 in MN9D cells (MN9D/PRX1) exerted neuroprotective effects against death induced by 6-OHDA through scavenging of ROS. Consequently, generation of both superoxide anion and hydrogen peroxide following 6-OHDA treatment was decreased in MN9D/PRX1. Furthermore, overexpression of PRX1 protected cells against 6-OHDA-induced activation of p38 MAPK and subsequent activation of caspase-3. In contrast, 6-OHDA-induced apoptotic death signals were enhanced by RNA interference-targeted reduction of PRX1 in MN9D cells. Taken together, our data suggest that the redox state of PRX may be intimately involved in 6-OHDA-induced dopaminergic neuronal cell death and also provide a molecular mechanism by which PRX1 exerts a protective role in experimental models of Parkinson disease.</P>