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Kim, Minx2010,Seok,Lee, Geunx2010,Hee,Kim, Yongx2010,Min,Lee, Byoungx2010,Wook,Nam, Hae Yun,Sim, Ux2010,Cheol,Choo, Sukx2010,Jung,Yu, Seongx2010,Woon,Kim, Jae‐,Joong,Kim Kwon, Yunh unknown 2017 Stem cells translational medicine Vol.6 No.6
<P><B>Abstract</B></P><P>Data are limited on the mechanisms underlying memory impairment in heart failure (HF). We hypothesized that angiotensin II (Ang II) may determine the fate of adult hippocampal neural stem cells (HCNs), a cause of memory impairment in HF. HCNs with neurogenesis potential were isolated and cultured from adult rat hippocampi. Ang II decreased HCN proliferation in dose‐ and time‐dependent manners. Moreover, Ang II treatment (1 µM) for 48 hours induced apoptotic death, which was attenuated by pretreatment with Ang II receptor blockers (ARBs). Ang II increased mitochondrial reactive oxygen species (ROS) levels, which was related to mitochondrial morphological changes and functional impairment. Moreover, ROS activated the AMP‐activated protein kinase (AMPK) and consequent peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC1α) expression, causing cell apoptosis. In the HF rat model induced by left anterior descending artery ligation, ARB ameliorated the spatial memory ability which decreased 10 weeks after ischemia. In addition, neuronal cell death, especially of newly born mature neurons, was observed in HF rat hippocampi. ARB decreased cell death and promoted the survival of newly born neural precursor cells and mature neurons. In conclusion, Ang II caused HCN apoptosis through mitochondrial ROS formation and subsequent AMPK‐PGC1α signaling. ARB improved learning and memory behaviors impaired by neuronal cell death in the HF animal model. These findings suggest that HCN is one treatment target for memory impairment in HF and that ARBs have additional benefits in HF combined with memory impairment. S<SMALL>TEM</SMALL> C<SMALL>ELLS</SMALL> T<SMALL>RANSLATIONAL</SMALL> M<SMALL>EDICINE</SMALL><I>2017;6:1491–1503</I></P>
Thermo‐sensitive nanogel‐laden bicontinuous microemulsion drug‐eluting contact lenses
Lee, Sex2010,Hee,Kim, Hox2010,Joong,Kim, Duckx2010,Hyun,Chang, Wonx2010,Seok,Vales, Temmy Pegarro,Kim, Jae‐,Woo,Kim, Kix2010,Hong,Kim, Jongx2010,Ki John Wiley Sons, Inc. 2019 Journal of Biomedical Materials Research Part B Vol.107 No.4
<P><B>Abstract</B></P><P>The bicontinuous microemulsion contact lens (BMCL) has nanoporous biphasic structures (100–250 nm) that are interconnected via multiple nano‐channels, providing suitable retention of various drugs for glaucoma. Timolol maleate (TM)‐carried thermosensitive poly(<I>N</I>‐isopropylacrylamide) (PNIPAM) nanogel (30–50 nm) was incorporated into BMCLs by soaking or by centrifuging plus soaking. Here, we present drug‐loading and release in silicon‐ or polyethylene oxide‐microemulsion BMCLs under various conditions. Nanoporous BMCLs containing thermosensitive TM‐laden nanogel were capable of potent body‐temperature‐triggered release of TM. Daily drug release was controllable according to the initial volume of drug‐loaded (VDL) and loading method for sustained drug release, making them reduce drug‐loss during transportation or storage. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 1159–1169, 2019.</P>
Evidence of carrier‐mediated transport in the penetration of donepezil into the rat brain
Kim, Mix2010,Hwa,Maeng, Hanx2010,Joo,Yu, Kyungx2010,Ha,Lee, Kyeongx2010,Ryoon,Tsuruo, Takashi,Kim, Daex2010,Duk,Shim, Changx2010,Koo,Chung, Sukx2010,Jae Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of Pharmaceutical Sciences Vol.99 No.3
<P><B>Abstract</B></P><P>The objective of this study was to characterize the mechanism that controls the transport of donepezil into the brain. The apparent brain uptake clearance (CL<SUB>app,br</SUB>) was decreased as a function of the dose of donepezil, suggesting an involvement of a saturable transport process via transporter(s) in the penetration across the blood–brain barrier (BBB). Consistent with <I>in vivo</I> results, the uptake of substrates for organic cation transporters was significantly reduced by donepezil in both MBEC4 cells (i.e., a model for BBB) and HEK 293 cells expressing the transporters found in the brain, indicative of the involvement of organic cation transporters in the transport of the drug. Furthermore, donepezil transport was enhanced (<I>p</I> < 0.01) in HEK 293 cells expressing rOCNT1, rOCTN2, or rCHT1. The CL<SUB>app,br</SUB> was reduced up to 52.8% of the control in rats that had been pretreated with choline, while the CL<SUB>app,br</SUB> was unaffected with pretreatments with organic cations other than choline, suggesting that choline and donepezil share a common transport mechanism in the penetration across the BBB <I>in vivo</I>. Taken together, these observations suggest that the transport of donepezil across the BBB is mediated by organic cation transporters such as choline transport system(s). © 2009 Wiley‐Liss, Inc. and the American Pharmacists Association J Pharm Sci 99: 1548–1566, 2010</P>
Lee, Kimoon,Oh, Min Suk,Mun, Sungx2010,jin,Lee, Kwang H.,Ha, Tae Woo,Kim, Jae Hoon,Park, Sangx2010,Hee Ko,Hwang, Chix2010,Sun,Lee, Byoung H.,Sung, Myung M.,Im, Seongil WILEY‐VCH Verlag 2010 Advanced Materials Vol.22 No.30
<P><B>Direct quantitative mapping of the density‐of‐states</B>, named the photo‐excited charge‐collection technique, for the interface traps at the n‐ZnO and/or p‐pentacene thin‐film transistor channel is implemented by using monochromatic photons which are carried by optical fibers and are probed onto thin‐film transistors. </P>
Kang, Lix2010,Jung,Kwon, Eunx2010,Soo,Lee, Kwang Min,Cho, Chanmi,Lee, Jae‐,In,Ryu, Young Bae,Youm, Tae Hyun,Jeon, Jimin,Cho, Mi Ra,Jeong, Seonx2010,Yong,Lee, Sangx2010,Rae,Kim, Wook,Yang John Wiley and Sons Inc. 2018 British journal of pharmacology Vol.175 No.23
<P><B>Background and Purpose</B></P><P>3′‐Sialyllactose (3′‐SL) is a safe compound that is present in high levels in human milk. Although it has anti‐inflammatory properties and supports immune homeostasis, its effect on collagen‐induced arthritis (CIA) is unknown. In this study, we investigated the prophylactic and therapeutic effect of 3′‐SL on the progression of rheumatoid arthritis (RA) in <I>in vitro</I> and <I>in vivo</I> models.</P><P><B>Experimental Approach</B></P><P>The anti‐arthritic effect of 3′‐SL was analysed with fibroblast‐like synoviocytes <I>in vitro</I> and an <I>in vivo</I> mouse model of CIA. RT‐PCR, Western blotting and ELISA were performed to evaluate its effects <I>in vitro</I>. Histological analysis of ankle and knee joints of mice with CIA was performed using immunohistochemistry, as well as safranin‐O and haematoxylin staining.</P><P><B>Key Results</B></P><P>3′‐SL markedly alleviated the severity of CIA in the mice by reducing paw swelling, clinical scores, incidence rate, serum levels of inflammatory cytokines and autoantibody production. Moreover, 3′‐SL reduced synovitis and pannus formation and suppressed cartilage destruction by blocking secretion of chemokines, pro‐inflammatory cytokines, https://en.wikipedia.org/wiki/Matrix_metalloproteinases and osteoclastogenesis <I>via</I> NF‐κB signalling. Notably, phosphorylation of p65, which is a key protein in the NF‐κB signalling pathway, was totally blocked by 3′‐SL in the RA models.</P><P><B>Conclusions and Implications</B></P><P>3′‐SL ameliorated pathogenesis of CIA by suppressing catabolic factor expression, proliferation of inflammatory immune cells and osteoclastogenesis. These effects were mediated <I>via</I> blockade of the NF‐κB signalling pathway. Therefore, 3′‐SL exerted prophylactic and therapeutic effects and could be a novel therapeutic agent for the treatment of RA.</P>
The lack of histological changes of CDMA cellular phone‐based radio frequency on rat testis
Lee, Haex2010,June,Pack, Jeongx2010,Ki,Kim, Taex2010,Hong,Kim, Nam,Choi, Soox2010,Yong,Lee, Jae‐,Seon,Kim, Sungx2010,Ho,Lee, Yunx2010,Sil Wiley Subscription Services, Inc., A Wiley Company 2010 Bioelectromagnetics Vol.31 No.7
<P><B>Abstract</B></P><P>We examined the histological changes by radiofrequency (RF) fields on rat testis, specifically with respect to sensitive processes such as spermatogenesis. Male rats were exposed to 848.5 MHz RF for 12 weeks. The RF exposure schedule consisted of two 45‐min RF exposure periods, separated by a 15‐min interval. The whole‐body average specific absorption rate (SAR) of RF was 2.0 W/kg. We then investigated correlates of testicular function such as sperm counts in the cauda epididymis, malondialdehyde concentrations in the testes and epididymis, frequency of spermatogenesis stages, germ cell counts, and appearance of apoptotic cells in the testes. We also performed p53, bcl‐2, caspase 3, p21, and PARP immunoblotting of the testes in sham‐ and RF‐exposed animals. Based on these results, we concluded that subchronic exposure to 848.5 MHz with 2.0 W/kg SAR RF did not have any observable adverse effects on rat spermatogenesis. Bioelectromagnetics 31:528–534, 2010. © 2010 Wiley‐Liss, Inc.</P>
Lee, Minx2010,Jae,Jung, Jieun,Na, Kyux2010,Hwan,Moon, Ji Suk,Lee, Heyx2010,Jin,Kim, Jae‐,Hwan,Kim, Gwang Il,Kwon, Sungx2010,Won,Hwang, Seongx2010,Gyu,Kim, Gi Jin Wiley Subscription Services, Inc., A Wiley Company 2010 Journal of cellular biochemistry Vol.111 No.6
<P><B>Abstract</B></P><P>Translational studies have explored the therapeutic effects of stem cells, raising hopes for the treatment of numerous diseases. Here, we evaluated the therapeutic effect of chorionic plate‐derived mesenchymal stem cells (CP‐MSCs) isolated from human placenta and transplanted into rats with carbon tetrachloride (CCl<SUB>4</SUB>)‐injured livers. CP‐MSCs were analyzed for hepatocyte‐specific gene expression, indocyanine green (ICG) uptake, glycogen storage, and urea production following hepatogenic differentiation. PKH26‐labeled CP‐MSCs were directly transplanted into the livers of rats that had been exposed to CCl<SUB>4</SUB> (1.6 g/kg, twice per week for 9 weeks). Blood and liver tissue were analyzed at 1, 2, and 3 weeks post‐transplantation. The expression of type I collagen (Col I) and matrix metalloproteinases (MMPs) was analyzed in rat T‐HSC/Cl‐6 hepatic stellate cells co‐cultured with CP‐MSCs following exposure to TGF‐β. The expression levels of α‐smooth muscle actin (α‐SMA) and Col I were lower in transplanted (TP) rats than in non‐transplanted (Non‐TP) animals (<I>P</I> < 0.05), whereas the expression levels of albumin and MMP‐9 were increased. TP rats exhibited significantly higher uptake/excretion of ICG than non‐TP rats (<I>P</I> < 0.005). In addition, collagen synthesis in T‐HSC/Cl‐6 cells exposed to TGF‐β was decreased by co‐culture with CP‐MSCs, which triggered the activation of MMP‐2 and MMP‐9. These results contribute to our understanding of the potential pathophysiological roles of CP‐MSCs, including anti‐fibrotic effects in liver disease, and provide a foundation for the development of new cell therapy‐based strategies for the treatment of difficult‐to‐treat liver diseases. J. Cell. Biochem. 111: 1453–1463, 2010. © 2010 Wiley‐Liss, Inc.</P>
Effects of 60 Hz 14 µT magnetic field on the apoptosis of testicular germ cell in mice
Kim, Yoonx2010,Won,Kim, Heex2010,Sung,Lee, Jinx2010,Sang,Kim, Youngx2010,Jin,Lee, Sangx2010,Kon,Seo, Jae‐,Nam,Jung, Kyeongx2010,Cheon,Kim, Nam,Gimm, Younx2010,Myoung Wiley Subscription Services, Inc., A Wiley Company 2009 BioElectroMagnetics Vol.30 No.1
<P><B>Abstract</B></P><P>We recently reported that continuous exposure, for 8 weeks, of extremely low frequency (ELF) magnetic field (MF) of 0.1 or 0.5 mT might induce testicular germ cell apoptosis in BALB/c mice. In that report, the ELF MF exposure did not significantly affect the body weight or testicular weight, but significantly increased the incidence of testicular germ cell death. In the present study, we aimed to further characterize the effect of a 16‐week continuous exposure to ELF MF of 14 or 200 µT on testicular germ cell apoptosis in mice. There were no significant effects of MF on body weight and testosterone levels in mice. In TUNEL staining (In situ terminal deoxynucleotidyl transferase‐mediated deoxy‐UTP nick end labeling), germ cells showed a significantly higher apoptotic rate in exposed mice than in sham controls (<I>P</I> < 0.001). TUNEL‐positive cells were mainly spermatogonia. In an electron microscopic study, degenerating spermatogonia showed condensation of nuclear chromatin similar to apoptosis. These results indicate that apoptosis may be induced in spermatogenic cells in mice by continuous exposure to 60 Hz MF of 14 µT. Bioelectromagnetics 30:66–72, 2009. © 2008 Wiley‐Liss, Inc.</P>
Kim, Jinx2010,Sik,Yeo, Seungeun,Shin, Dongx2010,Gu,Bae, Yoex2010,Sik,Lee, Jae‐,Jin,Chin, Byungx2010,Rho,Lee, Chux2010,Hee,Baek, Sukx2010,Hwan Blackwell Publishing Ltd 2010 FEBS JOURNAL Vol.277 No.13
<P>Macrophage activation contributes to the pathogenesis of atherosclerosis. In the vascular system, the major source of reactive oxygen species is the NADPH oxidase (Nox) family. Nox1 is induced by lipopolysaccharide (LPS) in macrophages, but the expression mechanism is not fully understood. We found that LPS causes β‐catenin accumulation by glycogen synthase kinase 3β (GSK3β) inactivation, and that β‐catenin accumulation increases Nox1 expression. LPS induced Nox1 mRNA expression and reactive oxygen species generation in Raw264.7 cells. Using bone marrow‐derived macrophages from toll‐like receptor 4 mutant mice, we also tested whether LPS‐induced Nox1 expression is toll‐like receptor 4 dependent. LPS caused GSK3β phosphorylation, induced β‐catenin accumulation and increased nuclear translocation. The GSK3β inhibitor LiCl potentiated LPS‐induced Nox1 expression in accordance with β‐catenin accumulation and nuclear translocation. Conversely, ectopic expression of a constitutively active GSK3β mutant severely attenuated Nox1 expression. These findings identify a novel regulatory pathway controlling Nox1 expression by LPS‐stimulated macrophages.</P>
Hwang, Ihx2010,Yeon,Sun, Eunx2010,Sun,An, Ji Hak,Im, Hana,Lee, Sunx2010,Ho,Lee, Joox2010,Yong,Han, Pyungx2010,Lim,Koh, Jae‐,Young,Kim, Yangx2010,Hee Blackwell Publishing Ltd 2011 Journal of Neurochemistry Vol.118 No.5
<P> <I>J. Neurochem.</I> (2011) <B>118</B>, 855–863.</P><P><B>Abstract</B></P><P>Tissue plasminogen activator (tPA) is necessary for hippocampal long‐term potentiation. Synaptically released zinc also contributes to long‐term potentiation, especially in the hippocampal CA3 region. Using cortical cultures, we examined whether zinc increased the concentration and/or activity of tPA. Two hours after a 10‐min exposure to 300 μM zinc, expression of tPA and its substrate, plasminogen, were significantly increased, as was the proteolytic activity of tPA. In contrast, increasing extracellular or intracellular calcium levels did not affect the expression or secretion of tPA. Changing zinc influx or chelating intracellular zinc also failed to alter tPA/plasminogen induction by zinc, indicating that zinc acts extracellularly. Zinc‐mediated extracellular activation of matrix metalloproteinase (MMP) underlies the up‐regulation of brain‐derived neurotrophic factor (BDNF) and tropomyosin receptor kinase (Trk) signaling. Consistent with these findings, co‐treatment with a neutralizing antibody against BDNF or specific inhibitors of MMPs or Trk largely reversed tPA/plasminogen induction by zinc. Treatment of cortical cultures with <I>p</I>‐aminophenylmercuric acetate, an MMP activator, MMP‐2, or BDNF alone induced tPA/plasminogen expression. BDNF mRNA and protein expression was also increased by zinc and mediated by MMPs. Thus, an extracellular zinc‐dependent, MMP‐ and BDNF‐mediated synaptic mechanism may regulate the levels and activity of tPA.</P>