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11.
Yoori Choi Kihwan Lee Junghwa Ryu Hyoun Geun Kim A Young Jeong Ran-Sook Woo Jun-Ho Lee Jin Won Hyun Seokyung Hahn Joung-Hun Kim Hye-Sun Kim 《PloS one》2014,9(8)
Neuritin, also known as CPG15, is a neurotrophic factor that was initially discovered in a screen to identify genes involved in activity-dependent synaptic plasticity. Neuritin plays multiple roles in the process of neural development and synaptic plasticity, although its binding receptor(s) and downstream signaling effectors remain unclear. In this study, we found that the cortical and hippocampal expression of neuritin is reduced in the brains of Alzheimer''s disease (AD) patients and demonstrated that viral-mediated expression of neuritin in the dentate gyrus of 13-month-old Tg2576 mice, an AD animal model, attenuated a deficit in learning and memory as assessed by a Morris water maze test. We also found that neuritin restored the reduction in dendritic spine density and the maturity of individual spines in primary hippocampal neuron cultures prepared from Tg2576 mice. It was also shown that viral-mediated expression of neuritin in the dentate gyrus of 7-week-old Sprague-Dawley rats increased neurogenesis in the hippocampus. Taken together, our results demonstrate that neuritin restores the reduction in dendritic spine density and the maturity of individual spines in primary hippocampal neurons from Tg2576 neurons, and also attenuates cognitive function deficits in Tg2576 mouse model of AD, suggesting that neuritin possesses a therapeutic potential for AD. 相似文献
12.
Park J Kim D Kim S Kim J Bae K Lee C 《Journal of microbiology and biotechnology》2007,17(7):1083-1089
Because of their selectivity and catalytic efficiency, BVMOs are highly valuable biocatalysts for the chemoenzymatic synthesis of a broad range of useful compounds. In this study, we investigated the microbial Baeyer-Villiger oxidation and sulfoxidation of thioanisole and bicyclo[3.2.0]hept-2-en-6-one using whole Escherichia coli cells that recombined with each of the Baeyer-Villiger monooxygenases originated from Pseudomonas aeruginosa PAO1 and two from Streptomyces coelicolor A3(2). The three BVMOs were identified in the microbial genome database by a recently described protein sequence motif; e.g., BVMO motif (FXGXXXHXXXW). The reaction products were identified as (R)-/(S)sulfoxide and 2-oxabicyclo/3-oxabicyclo[3.3.0]oct-6-en-2-one by GC-MS analysis. Consequently, this study demonstrated that the three enzymes can indeed catalyze the Baeyer-Villiger reaction as a biocatalyst, and effective annotation tools can be efficiently exploited as a source of novel BVMOs. 相似文献
13.
Falck JR Reddy LM Byun K Campbell WB Yi XY 《Bioorganic & medicinal chemistry letters》2007,17(9):2634-2638
Eight members of a recently identified family of tetrahydrofuran-diols (THFDs), originating from epoxyeicosatrienoic acids (EETs), were prepared stereospecifically from D-(+)-glucose. The THFDs potently induced relaxation of pre-contracted bovine arteries. 相似文献
14.
A naturally occurring bile acid, ursodeoxycholic acid (UDCA), is known to alleviate endoplasmic reticulum (ER) stress at the cellular level. However, the detailed action mechanisms of UDCA in atherosclerosis are not fully understood. In this study, we demonstrated whether UDCA exerts anti-atherogenic activity in diabetic atherosclerosis by targeting ER stress and “receptor for advanced glycation endproduct” (RAGE) signaling. UDCA markedly reduced ER stress, RAGE expression, and pro-inflammatory responses [including NF-κB activation and reactive oxygen species (ROS) production] induced in endothelial cells (ECs) by high glucose (HG). In particular, UDCA inhibited HG-induced ROS production by increasing the Nrf2 level. In macrophages, UDCA also blocked HG-induced RAGE and pro-inflammatory cytokine expression and inhibited foam cell formation via upregulation of the ATP-binding cassette (ABC) transporters, ABCA1 and ABCG1. In the diabetic mouse model, UDCA inhibited atheromatous plaque formation by decreasing ER stress, and the levels of RAGE and adhesion molecules. In conclusion, UDCA exerts an anti-atherogenic activity in diabetic atherosclerosis by targeting both ER stress and RAGE signaling. Our work implicates UDCA as a potential therapeutic agent for prevention or treatment of diabetic atherosclerosis. 相似文献
15.
Kim Soo J. Baik Inkyung Kim Jehyeong Jung Kihwan Lee Seung H. Kim Se J. Shin Chol 《Sleep and biological rhythms》2010,8(2):144-150
Sleep and Biological Rhythms - Obesity is consistently reported to have a positive association with the development of habitual snoring. Whether lifestyle factors modify the association between... 相似文献
16.
Lee I Ahn B Choi J Hattori M Min B Bae K 《Bioorganic & medicinal chemistry letters》2011,21(21):6603-6607
Two new lanostane triterpenes, named methyl ganoderate A acetonide (1) and n-butyl ganoderate H (2), were isolated from the fruiting bodies of Ganoderma lucidum together with 16 known compounds (3-18). Extensive spectroscopic and chemical studies established the structures of these compounds as methyl 7β,15α-isopropylidenedioxy-3,11,23-trioxo-5α-lanost-8-en-26-oate (1) and n-butyl 12β-acetoxy-3β-hydroxy-7,11,15,23-tetraoxo-5α-lanost-8-en-26-oate (2). Because new compounds exhibiting specific anti-acetylcholinesterase activity are being sought as possible drug candidates for the treatment of Alzheimer's and related neurodegenerative diseases, compounds 1-18 were examined for their inhibitory activities against acetylcholinesterase and butyrylcholinesterase. All of the compounds exhibited moderate acetylcholinesterase-inhibitory activity, with IC(50) values ranging from 9.40 to 31.03μM. In contrast, none of the compounds except lucidadiol (13) and lucidenic acid N (14) exhibited butyrylcholinesterase-inhibitory activity at concentrations up to 200μM. These results indicate that these lanostane triterpenes are preferential inhibitors of acetylcholinesterase and may be suitable drug candidates. 相似文献
17.
Dong Hoon Kang Mina Choi Soyoung Chang Min Young Lee Doo Jae Lee Kyungsun Choi Junseong Park Eun Chun Han Daehee Hwang Kihwan Kwon Hanjoong Jo Chulhee Choi Sang Won Kang 《PloS one》2015,10(8)
Neointimal hyperplasia of vascular smooth muscle cells (VSMC) plays a critical role in atherosclerotic plaque formation and in-stent restenosis, but the underlying mechanisms are still incompletely understood. We performed a proteomics study to identify novel signaling molecules organizing the VSMC hyperplasia. The differential proteomics analysis in a balloon-induced injury model of rat carotid artery revealed that the expressions of 44 proteins are changed within 3 days post injury. The combination of cellular function assays and a protein network analysis further demonstrated that 27 out of 44 proteins constitute key signaling networks orchestrating the phenotypic change of VSMC from contractile to epithelial-like synthetic. Among the list of proteins, the in vivo validation specifically revealed that six proteins (Rab15, ITR, OLR1, PDHβ, PTPε) are positive regulators for VSMC hyperplasia. In particular, the OLR1 played dual roles in the VSMC hyperplasia by directly mediating oxidized LDL-induced monocyte adhesion via NF-κB activation and by assisting the PDGF-induced proliferation/migration. Importantly, OLR1 and PDGFRβ were associated in close proximity in the plasma membrane. Thus, this study elicits the protein network organizing the phenotypic change of VSMC in the vascular injury diseases such as atherosclerosis and discovers OLR1 as a novel molecular link between the proliferative and inflammatory responses of VSMCs. 相似文献
18.
Mitogen-activated protein kinase (MAPK) cascades are central components of the intracellular signaling networks used by eukaryotic cells to respond to a wide spectrum of extracellular stimuli. An MAPK is activated by an MAPK kinase, which in turn is activated by an MAPK kinase kinase (MAP3K). However, little is known about the molecular aspects of the regulation and activation of large numbers of MAP3Ks that are crucial in relaying upstream receptor-mediated signals through the MAPK cascades to induce various physiological responses. In this study, we identified a novel MEKK2-interacting protein, Mip1, that regulates MEKK2 dimerization and activation by forming a complex with inactive and nonphosphorylated MEKK2. In particular, Mip1 prevented MEKK2 activation by blocking MEKK2 dimer formation, which in turn blocked JNKK2, c-Jun N-terminal kinase 1 (JNK1), extracellular signal-regulated kinase 5, and AP-1 reporter gene activation by MEKK2. Furthermore, we found that the endogenous Mip1-MEKK2 complex was dissociated transiently following epidermal growth factor stimulation. In contrast, the knockdown of Mip1 expression by siRNA augmented the MEKK2-mediated JNK and AP-1 reporter activation. Together, our data suggest a novel model for MEKK2 regulation and activation. 相似文献
19.
Cheonjae Yoon Kihwan Lim Sungjun Lee Yanghwan Choi Youngwhan Choi Jungsuk Lee 《Cell and tissue banking》2016,17(1):21-31
Human skin allografts are one of the best temporary biological coverings for severely burned patients. Cryopreserved (CPA) and glycerol-preserved (GPA) allografts are the most widely used types. This study compared the allograft efficiency of both preservation methods under the same conditions. To simulate actual clinical conditions, we used a porcine wound model. In addition, we evaluated the macroscopic and microscopic scoring of graft performance for each method. Porcine cadaver skin 1 mm thick was obtained from one pig. Cryopreserved skin cell viability was 20.8 %, glycerol-preserved skin was 9.08 %, and fresh skin was 58.6 %. We made ten partial-thickness wounds each in two pigs. The take rates on day 2 were 96.23 and 82.65 % in the GPA and CPA group (both n = 9), respectively. After 1 week, the take rates of both groups were nearly equal. The removal rate at week 5 was 98.87 and 94.41 % in the GPA and CPA group, respectively. On microscopic findings at week 2, inflammation was greater in the CPA group. Other findings such as fibroblast hyperplasia and neovascularization were not significantly different between both groups. At week 5, the score of collagen fiber synthesis was 2.67 ± 0.47 and 2.33 ± 0.47 in the GPA and CPA group, respectively. The epidermal-dermal junction was 2.22 ± 0.79 and 2.00 ± 0.47 in the GPA and CPA group, respectively. These findings suggest that wound healing takes longer in the CPA group. The preservation method of allografts is not a absolute factor in the wound healing process in this wound model. 相似文献
20.
Khin Thanda Win Juan Vegas Chunying Zhang Kihwan Song Sanghyeob Lee 《TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik》2017,130(1):199-211