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사람 태아 성장세포에서 종양괴사인자 유전자 발현의 조절
류혜명,박주영,최선주,박현숙,고춘명,Ryu, Hye-Myung,Park, Joo-Young,Choi, Sun-Ju,Park, Hyun-Sook,Koh, Choon-Myung 대한미생물학회 2001 Journal of Bacteriology and Virology Vol.31 No.3
Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) involved in the pathogenesis of multiple sclerosis and contribute to the degeneration of oligodendrocytes as well as neurons. TNF-${\alpha}$ is produced by miocroglia and astrocytes, which also produce hormones and cytokines that influence its biological activity. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-${\alpha}$ at both the mRNA and protein levels in response to interleukine-1 (IL-1) or TNF-${\alpha}$. Two immunosuppressive cytokines, transforming growth factor-${\beta}$ (TGF-${\beta}$) and IL-10, have been shown to influence glial cell function. TGF-${\beta}$ can modulate the activity of glial cells by inhibiting interferon-${\gamma}$ (IFN-${\gamma}$) induced expression of class II major histocompatibility complex (MHC) molecules on astrocytes and microglia. To explore the role of astrocytes in the production of TNF-${\alpha}$, astrocytes were pretreated with IL-10 or TGF-${\beta}$ and then stimulated with IL-1${\beta}$ to determine their effects on TNF-${\alpha}$ production. The secretion of TNF-${\alpha}$ by human fetal astrocytes was markedly inhibited by TGF-${\beta}$ at a low concentration. In contrast IL-10 had no effect on TNF-${\alpha}$ mRNA level. These results show that TGF-${\beta}$ may regulate the expression of TNF-${\alpha}$ in activated human fetal astrocytes.
류혜명,최순윤,김용림 계명대학교 자연과학연구소 2015 Quantitative Bio-Science Vol.34 No.1
Recombinant human erythropoietin (EPO), a glycohormone, is one of the leading biopharmaceutical products, while carbamylated erythropoietin (CEPO), an EPO derivative, is attracting widespread interest due to its neuroprotective effects without erythropoiesis in several cells and animal models. However, the protective effects of CEPO on renal fibrosis still remain unknown. In this study, we evaluated the inhibitory effects of CEPO against transforming growth factor (TGF)-β1-induced epithelial-to-mesenchymal transition (EMT) in Madin-Darby Canine Kidney (MDCK) cells. MDCK cells were treated with TGF-β1 (5 ng/mL) for 48 h to induce EMT, and the cells were then co-treated with TGF-β1 and CEPO or recombinant human EPO for another 48 h. Increased expressions of α-smooth muscle actin (α-SMA) and decreased expressions of E-cadherin were observed after TGF-β1 treatment, and these changes were markedly attenuated by CEPO co-treatment. TGF-β1 increased phosphorylated Smad-2 expression in MDCK cells, which was decreased by CEPO cotreatment. The results indicate that CEPO ameliorates the TGF-β1-induced EMT mediated by p-Smad2 pathway. It suggests that CEPO has therapeutic potential in chronic kidney disease.
The Frequency of MSI in Unselected Korean Colorectal Adenocarcinomas
류혜명,--,-- THE KOREAN SOCIETY FOR BIOMEDICAL LABORATORY SCIEN 2003 Journal of biomedical laboratory sciences Vol.9 No.3
Microsatellite instability (MSI), which is caused by a deficient mismatch repair system, is seen in most of the hereditary non-polyposis colon cancers (HNPCC) and a portion of sporadic colorectal cancers. Forty unselected colorectal cancer patients were analyzed for MSI using silver stain plus kit. The overall incidence of MSI in studied cases was 17% (7/40). The incidence is similar result with previous study. MSI in colorectal carcers was more prevalent in moderative differentiated adenocarcinoma than well differentiated adenocarcinoma.
Fimasartan attenuates renal ischemia-reperfusion injury by modulating inflammation-related apoptosis
조장희,최순윤,류혜명,오은주,육주민,안지선,정희연,최지영,박선희,김찬덕,김용림 대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.6
Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor (TNF)-α, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of TNF-α, interleukin (IL)-1β, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.
생쥐의 배자에서 위치 특이적 발현을 보이는 새로운 유전자의 분리
김명희,박형우,류혜명 한국유전학회 2000 Genes & Genomics Vol.22 No.2
During embryonic development, cells signal to each other, regulate the fates of cells, and eventually form a pattern of a particular animal. To isolate novel signalling developmental control genes, differential display (DD) RT-PCR was performed. Mouse embryos at the mid-gastrulation stage were isolated and sliced into eight pieces along the anterior-posterior (A-P) axis, and total RNAs were isolated from each segment and used for DDRT-PCR. The bands expressed differentially (decreasing or increasing expression along the axis, or head-, trunk- or tail-specific expression, etc.) along the A-P axis were selected and the cDNAs were analyzed after subcloning and sequencing. Out of 20 clones analyzed 9 clones turned out to be known developmental control genes such as forkhead-1, α-tropomyosin, Hoxd-11, sfrp-1 etc., whereas 11 were novel that have not yet been identified thus far. Most of the known genes screened here were developmentally regulated and differentially expressed during embryogenesis so that the novel genes could be good candidates for developmental control genes: two novel genes, G8B1 and C1A1 cloned from the head region, were expressed in temporally restricted manner, besides spatially restricted pattern of expression. These results altogether suggest that the novel genes expressed position-specifically during mid-gastrulation stage are likely to be putative developmental control genes which are involved in signalling the developmental cascade finally leading to a particular pattern of an animal.
이문희,이명훈,류혜명,유민 대한의생명과학회 2007 Biomedical Science Letters Vol.13 No.3
P2X receptors are membrane-bound ion channels that conduct Na+, K+, and Ca2+ in response to ATP and its analogs. There are seven subunits identified so far (P2X1-P2X7). P2X2 receptors are known to be expressed in a wide range of organs including brains and adrenal grands. PC12 cells are originated from adrenal grand and differentiated by nerve growth factor or pituitary adenylate cyclase activating poly peptide (PACAP). Previous studies indicate that P2X2 receptor activation in PC12 cells couples to Ca2+-dependent release of catecholamine and ATP. It is known that acidic pH potentiates ATP currents at P2X2 receptors. This leads to a hypothesis that P2X2 receptors may play an important role in PC12 cell differentiation, one of the characteristics of which is neurite outgrowth, induced by the hormones under lower pH. In the present study, we isolated several clones which potentiate neurite outgrowth by PACAP in acidic pH (6.8), but not in alkaline pH (7.6). RT-PCR and electrophysiology data indicate that these clones express only functional P2X2 receptors in the absence or presence of PACAP for 3 days. Potentiation of neurite outgrowth resulted from PACAP (100 nM) in acidic pH is inhibited by the two P2X receptor antagonists, suramin and PPADS (100 μM each), and exogenous exprerssion of ATP-binding mutant P2X2 receptor subunit (P2X2[K69A]). However, acid sensing ion channels (ASICs) are not involved in PACAP-induced neurite outgrowth potentiation in lower pH since treatments of an inhibitor of ASICs, amyloride (10 μM), did not give any effects to neurite extension. The vesicular proton pump (H+-ATPase) inhibitor, bafilomycin (100 nM), reduced neurite extension indicating that ATP release resulted from P2X2 receptor activation in PC12 cells is needed for neurite outgrowth. These were confirmed by activation of mitogen activated protein kinases, such as ERKs and p38. These results suggest roles of ATP and P2X2 receptors in hormoneinduced cell differentiation or neuronal synaptogenesis in local acidic environments.