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Jang, Youngx2010,Ho,Kim, Junex2010,Hong,Ban, Changill,Ahn, Kyohan,Cheong, Jaex2010,Hun,Kim, Hyungx2010,Hoi,Kim, Jungx2010,Soo,Park, Yongx2010,Hyun,Kim, Jun,Chun, Kookx2010,Jin,Lee, Gyeon Blackwell Publishing Ltd 2012 CARDIOVASCULAR THERAPEUTICS Vol.30 No.5
<P><B>SUMMARY</B></P><P>Recent studies have shown that stromal cell derived factor‐1 (SDF‐1), first known as a cytokine involved in recruiting stem cells into injured organs, confers myocardial protection in myocardial infarction, which is not dependent on stem cell recruitment but related with modulation of ischemia‐reperfusion (I/R) injury. However, the effect of SDF has been studied only in a preischemic exposure model, which is not clinically relevant if SDF is to be used as a therapeutic agent. Our study was aimed at evaluating whether or not SDF‐1 confers cardioprotection during the reperfusion period. Hearts from SD rats were isolated and perfused with the Langendorff system. Proximal left coronary artery ligation, reperfusion, and SDF perfusion in KH buffer was done according to study protocol. Area of necrosis (AN) relative to area at risk (AR) was the primary endpoint of the study. Significant reduction of AN/AR by SDF in an almost dose‐dependent manner was noted during both the preischemic exposure and reperfusion periods. In particular, infusion of a high concentration of SDF (25 nM/L) resulted in a dramatic reduction of infarct size, which was greater than that achieved with ischemic pre‐ or postconditioning. SDF perfusion during reperfusion was associated with a similar significant reduction of infarct size as preischemic SDF exposure. Further studies are warranted to assess the potential of SDF as a therapeutic agent for reducing I/R injury in clinical practice.</P>
Yang, Kyeong Eun,Jang, Hyunx2010,Jin,Hwang, Inx2010,Hu,Chung, Youngx2010,Ho,Choi, Jongx2010,Soon,Lee, Taex2010,Hoon,Chung, Yunx2010,Jo,Lee, Minx2010,Seung,Lee, Mi Young,Yeo, Euix2010,J BLACKWELL PUBLISHING 2016 AGING CELL Vol.15 No.2
<P><B>Summary</B></P><P>Phenyl‐2‐pyridyl ketoxime (PPKO) was found to be one of the small molecules enriched in the extracellular matrix of near‐senescent human diploid fibroblasts (HDFs). Treatment of young HDFs with PPKO reduced the viability of young HDFs in a dose‐ and time‐dependent manner and resulted in senescence‐associated β‐galactosidase (SA‐β‐gal) staining and G2/M cell cycle arrest. In addition, the levels of some senescence‐associated proteins, such as phosphorylated ERK1/2, caveolin‐1, p53, p16<SUP>ink4a</SUP>, and p21<SUP>waf1</SUP>, were elevated in PPKO‐treated cells. To monitor the effect of PPKO on cell stress responses, reactive oxygen species (ROS) production was examined by flow cytometry. After PPKO treatment, ROS levels transiently increased at 30 min but then returned to baseline at 60 min. The levels of some antioxidant enzymes, such as catalase, peroxiredoxin II and glutathione peroxidase I, were transiently induced by PPKO treatment. SOD II levels increased gradually, whereas the SOD I and III levels were biphasic during the experimental periods after PPKO treatment. Cellular senescence induced by PPKO was suppressed by chemical antioxidants, such as N‐acetylcysteine, 2,2,6,6‐tetramethylpiperidinyloxy, and L‐buthionine‐(<I>S</I>,<I>R</I>)‐sulfoximine. Furthermore, PPKO increased nitric oxide (NO) production via inducible NO synthase (iNOS) in HDFs. In the presence of NOS inhibitors, such as L‐NG‐nitroarginine methyl ester and L‐NG‐monomethylarginine, PPKO‐induced transient NO production and SA‐β‐gal staining were abrogated. Taken together, these results suggest that PPKO induces cellular senescence in association with transient ROS and NO production and the subsequent induction of senescence‐associated proteins<B>.</B></P>
DMSO‐ and Serum‐Free Cryopreservation of Wharton's Jelly Tissue Isolated From Human Umbilical Cord
Shivakumar, Sharath Belame,Bharti, Dinesh,Subbarao, Raghavendra Baregundi,Jang, Six2010,Jung,Park, Jix2010,Sung,Ullah, Imran,Park, Jix2010,Kwon,Byun, Junex2010,Ho,Park, Bongx2010,Wook,Rho, G John Wiley and Sons Inc. 2016 Journal of cellular biochemistry Vol.117 No.10
<P><B>ABSTRACT</B></P><P>The facile nature of mesenchymal stem cell (MSC) acquisition in relatively large numbers has made Wharton's jelly (WJ) tissue an alternative source of MSCs for regenerative medicine. However, freezing of such tissue using dimethyl sulfoxide (DMSO) for future use impedes its clinical utility. In this study, we compared the effect of two different cryoprotectants (DMSO and cocktail solution) on post‐thaw cell behavior upon freezing of WJ tissue following two different freezing protocols (Conventional [−1°C/min] and programmed). The programmed method showed higher cell survival rate compared to conventional method of freezing. Further, cocktail solution showed better cryoprotection than DMSO. Post‐thaw growth characteristics and stem cell behavior of Wharton's jelly mesenchymal stem cells (WJMSCs) from WJ tissue cryopreserved with a cocktail solution in conjunction with programmed method (Prog‐Cock) were comparable with WJMSCs from fresh WJ tissue. They preserved their expression of surface markers, pluripotent factors, and successfully differentiated in vitro into osteocytes, adipocytes, chondrocytes, and hepatocytes. They also produced lesser annexin‐V‐positive cells compared to cells from WJ tissue stored using cocktail solution in conjunction with the conventional method (Conv‐Cock). Real‐time PCR and Western blot analysis of post‐thaw WJMSCs from Conv‐Cock group showed significantly increased expression of pro‐apoptotic factors (BAX, p53, and p21) and reduced expression of anti‐apoptotic factor (BCL2) compared to WJMSCs from the fresh and Prog‐Cock group. Therefore, we conclude that freezing of fresh WJ tissue using cocktail solution in conjunction with programmed freezing method allows for an efficient WJ tissue banking for future MSC‐based regenerative therapies. J. Cell. Biochem. 117: 2397–2412, 2016. © 2016 The Authors. <I>Journal of Cellular Biochemistry</I> published by Wiley Periodicals, Inc.</P>
Won, Cheolhee,Kim, Byungx2010,Hak,Yi, Eun Hee,Choi, Kyungx2010,Ju,Kim, Eunx2010,Kyung,Jeong, Jongx2010,Min,Lee, Jaex2010,Ho,Jang, Jax2010,June,Yoon, Jungx2010,Hwan,Jeong, Wonx2010,Il,P John Wiley and Sons Inc. 2015 Hepatology Vol.62 No.4
<P>Enhanced expression of the cancer stem cell (CSC) marker, CD133, is closely associated with a higher rate of tumor formation and poor prognosis in hepatocellular carcinoma (HCC) patients. Despite its clinical significance, the molecular mechanism underlying the deregulation of CD133 during tumor progression remains to be clarified. Here, we report on a novel mechanism by which interleukin‐6/signal transducer and activator of transcription 3 (IL‐6/STAT3) signaling up‐regulates expression of CD133 and promotes HCC progression. STAT3 activated by IL‐6 rapidly bound to CD133 promoter and increased protein levels of CD133 in HCC cells. Reversely, in hypoxic conditions, RNA interference silencing of STAT3 resulted in decrease of CD133 levels, even in the presence of IL‐6, with a concomitant decrease of hypoxia‐inducible factor 1 alpha (HIF‐1α) expression. Active STAT3 interacted with nuclear factor kappa B (NF‐κB) p65 subunit to positively regulate the transcription of HIF‐1α providing a mechanistic explanation on how those three oncogenes work together to increase the activity of CD133 in a hypoxic liver microenvironment. Activation of STAT3 and its consequent induction of HIF‐1α and CD133 expression were not observed in Toll‐like receptor 4/IL‐6 double‐knockout mice. Long‐term silencing of CD133 by a lentiviral‐based approach inhibited cancer cell‐cycle progression and suppressed <I>in vivo</I> tumorigenicity by down‐regulating expression of cytokinesis‐related genes, such as TACC1, ACF7, and CKAP5. We also found that sorafenib and STAT3 inhibitor nifuroxazide inhibit HCC xenograft formation by blocking activation of STAT3 and expression of CD133 and HIF‐1α proteins. <I>Conclusion</I>: IL‐6/STAT3 signaling induces expression of CD133 through functional cooperation with NF‐κB and HIF‐1α during liver carcinogenesis. Targeting STAT3‐mediated CD133 up‐regulation may represent a novel, effective treatment by eradicating the liver tumor microenvironment. (H<SMALL>EPATOLOGY</SMALL> 2015;62:1160‐1173)</P>
Hong, Mi Jeong,Yoo, Seung Soo,Choi, Jin Eun,Kang, Hyox2010,Gyoung,Do, Sook Kyung,Lee, Jang Hyuck,Lee, Won Kee,Lee, Jaehee,Lee, Shin Yup,Cha, Seung Ick,Kim, Chang Ho,Lee, Eung Bae,Cho, Sukki,Jheon, S John Wiley and Sons Inc. 2018 Cancer Science Vol.109 No.12
<P>RegulomeDB is a new tool that can predict the regulatory function of genetic variants. We applied RegulomeDB in selecting putative functional variants and evaluated the relationship between these variants and survival outcomes of surgically resected non‐small‐cell lung cancer. Among the 244 variants studied, 14 were associated with overall survival (<I>P </I><<I> </I>0.05) in the discovery cohort and one variant (rs2257609 C>T) was replicated in the validation cohort. In the combined analysis, rs2257609 C>T was significantly associated with worse overall and disease‐free survival under a dominant model (<I>P </I>=<I> </I>2 × 10<SUP>−5</SUP> and <I>P </I>=<I> </I>0.001, respectively). rs2257609 is located in the <I>SLC5A10</I> intron, but RegulomeDB predicted that this variant affected <I>DRG2</I>, not <I>SLC5A10</I> expression. The expression level of <I>SLC5A10</I> was not different with the rs2257609 genotype. However, <I>DRG2</I> expression was different according to the rs2257609 genotype (<I>P</I><SUB>trend</SUB><SUP> </SUP>= 0.03) and was significantly higher in tumor than in non‐malignant lung tissues (<I>P </I>=<I> </I>1 × 10<SUP>−5</SUP>). Luciferase assay also showed higher promoter activity of <I>DRG2</I> in samples with the rs2257609 T allele (<I>P </I><<I> </I>0.0001). rs2257609 C>T affected <I>DRG2</I> expression and, thus, influenced the prognosis of early‐stage non‐small‐cell lung cancer. This study was approved by the Institutional Review Broad of Kyungpook National University of Hospital (Approval No. KNUMC 2014‐04‐210‐003).</P>
Jang, Kukx2010,In,Shim, Miseon,Lee, Sang Min,Huh, Hyu Jung,Huh, Seung,Joo, Jix2010,Young,Lee, Seungx2010,Hwan,Chae, Jeongx2010,Ho John Wiley Sons Australia, Ltd 2017 PSYCHIATRY AND CLINICAL NEUROSCIENCES Vol.71 No.11
<P>Conclusion: This study suggests that increased beta power, reflecting the psychopathology in the bereaved families of the Sewol ferry disaster, may be a compensatory mechanism that follows complex trauma. Frontal beta power could be a potential marker indicating the severity of sleep disturbances. Our results suggest that sleep disturbance is an important symptom in family members of the Sewol ferry disaster's victims, which may be screened by EEG beta power.</P>
Non‐Volatile Control of 2DEG Conductivity at Oxide Interfaces
Kim, Shinx2010,Ik,Kim, Daix2010,Hong,Kim, Yoonjung,Moon, Seon Young,Kang, Minx2010,Gyu,Choi, Jong Kwon,Jang, Ho Won,Kim, Seong Keun,Choi, Jix2010,Won,Yoon, Seokx2010,Jin,Chang, Hye Jung,Kang WILEY‐VCH Verlag 2013 ADVANCED MATERIALS Vol.25 No.33
<P><B>The functionalization of two‐dimensional electron gas (2DEG) at oxide interfaces</B> can be realized integrating 2DEG with multifunctional oxide overlayers by epitaxial growth. Using a ferroelectric Pb(Zr<SUB>0.2</SUB>Ti<SUB>0.8</SUB>)O<SUB>3</SUB> overlayer on 2DEG (LaAlO<SUB>3</SUB>/SrTiO<SUB>3</SUB>), we demonstrate a model system of the functionalized 2DEG, where electrical conductivity of 2DEG can be reversibly controlled with a large on/off ratio (>1000) in a non‐volatile way by ferroelectric polarization switching.</P>
Lee, Eun Jung,Heo, Woo Choul,Park, Jang Woo,Chang, Yongmin,Bae, Jix2010,Eun,Chae, Kwon Seok,Kim, Tae Jeong,Park, Ji Ae,Lee, Gang Ho WILEY‐VCH Verlag 2013 European journal of inorganic chemistry Vol.2013 No.16
<P>To date, only a few nanosystems have been investigated as T1 MRI-CT dual contrast agents. The T1 MRI-CT dual functionality of a material depends on its longitudinal water-proton relaxivity (r1) and X-ray absorption strength. We explored Gd(IO3)3 center dot 2H2O nanomaterial because Gd is the most powerful element for T1 MRI contrast agents, and both Gd and I absorb X-ray radiation; Gd absorbs X-ray radiation ca. 2.5 times more strongly than I. D-Glucuronic acid coated Gd(IO3)3 center dot 2H2O nanomaterial showed a very large r1 of 52.3 s1mM1 (r2/r1 = 1.21), which could be ascribed to hydrated water molecules in the lattice. Its X-ray absorption intensity was also stronger than those of commercial molecular iodine CT contrast agents. This result clearly suggests that D-glucuronic acid coated Gd(IO3)3 center dot 2H2O nanomaterial is a potential T1 MRI-CT dual contrast agent.</P>
O‐GlcNAcase is essential for embryonic development and maintenance of genomic stability
Yang, Yong Ryoul,Song, Minseok,Lee, Ho,Jeon, Yoon,Choi, Eunx2010,Jeong,Jang, Hyunx2010,Jun,Moon, Hyo Youl,Byun, Hax2010,Young,Kim, Eungx2010,Kyun,Kim, Dae Hyun,Lee, Mi Nam,Koh, Ara,Ghim, Jaewa Blackwell Publishing Ltd 2012 Aging cell Vol.11 No.3
<P><B>Summary</B></P><P>Dysregulation of O‐GlcNAc modification catalyzed by O‐GlcNAc transferase (OGT) and O‐GlcNAcase (OGA) contributes to the etiology of chronic diseases of aging, including cancer, cardiovascular disease, type 2 diabetes, and Alzheimer’s disease. Here we found that natural aging in wild‐type mice was marked by a decrease in OGA and OGT protein levels and an increase in O‐GlcNAcylation in various tissues. Genetic disruption of OGA resulted in constitutively elevated O‐GlcNAcylation in embryos and led to neonatal lethality with developmental delay. Importantly, we observed that serum‐stimulated cell cycle entry induced increased O‐GlcNAcylation and decreased its level after release from G2/M arrest, indicating that O‐GlcNAc cycling by OGT and OGA is required for precise cell cycle control. Constitutively, elevated O‐GlcNAcylation by OGA disruption impaired cell proliferation and resulted in mitotic defects with downregulation of mitotic regulators. OGA loss led to mitotic defects including cytokinesis failure and binucleation, increased lagging chromosomes, and micronuclei formation. These findings suggest an important role for O‐GlcNAc cycling by OGA in embryonic development and the regulation of the maintenance of genomic stability linked to the aging process.</P>
Kim, Gunx2010,Dong,Kim, Taex2010,Ho,Jang, Anx2010,Hee,Ahn, Hyunx2010,Jong,Park, Yong Seek,Park, Cheungx2010,Seog Blackwell Publishing Ltd 2011 Experimental dermatology Vol.20 No.2
<P><B>Abstract: </B> Atopic dermatitis (AD) is a common skin disease that has complex pathogenic mechanisms. Under specific pathogen‐free conditions, repeated epicutaneous treatment of 2‐4‐dinitrofluorobenzene (DNFB) evokes AD‐like clinical symptoms in NC/Nga mice. α‐Lipoic acid (α‐LA; 1, 2‐dithiolane‐3‐pentanoic acid) is a dietary component that is synthesized in bacteria, yeast, plants, and mammals. α‐LA and its reduced form, dihydrolipoic acid, are powerful antioxidants that have many physiological functions, including free radical scavenging of reactive oxygen species, generation of cellular antioxidants, chelation of metal ions, and inflammatory suppression. In this study, we investigated whether α‐LA suppresses AD‐like skin lesions induced by repeated DNFB application in NC/Nga mice. α‐LA significantly suppressed production of interferon (IFN)‐γ and interleukin (IL)‐4 by activated CD4<SUP>+</SUP> T cells. We found that the oral administration of α‐LA reduced AD‐like clinical symptoms and inhibited increases of epidermal thickness in DNFB‐induced AD‐like skin lesions of NC/Nga mice. Furthermore, total serum IgE levels were dramatically reduced by topical α‐LA treatment. Our findings suggest that oral administration of α‐LA suppresses the development of AD in DNFB‐treated NC/Nga mice and reduces IFN‐γ and IL‐4 production from activated CD4<SUP>+</SUP> T cells as well as total serum IgE levels.</P>