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Native LDL induces IL-8 upregulation and cell proliferation in VSMC
허광래 이화여자대학교 세포신호전달연구센터 2005 고사리 세포신호전달 심포지움 Vol. No.7
High blood level of low-densitylipoprotein(LDL) is well known as a risk factor for atherogenesis. Migration and proliferation of vascular smooth muscle cells(VSMC) are closely associated with atherosclerosis. Therefore, a group of genes was found by PCR-based cDNA subtraction between LDL-treated group and non-treated group. Northern blot analysis was performed to find genes including interleukin-8 differentially expressed in hyperlipidemic conditions. LDL-induced IL-8 expression is specific to SMCs and likely to be regulated at the transcriptional level in dose- and time-dependent manners, as judged by RT-PCR and ELISA analyses in the presence of actinomycin D. The LDL signal is likely to be mediated by an unidentified pertussis toxin (PTX)sensitive receptor(s), since pretreatment with PTX, but not heparin, genistein, cholera toxin, BN52021, lysophophatic acid, and sphingosine-1-phosphate, abolished LDL-stimulated IL-8 induction. Although both p38 mitogen-activated proteinkinases(MAPKs) and extracellular signal-regulated kinase(Erk) 1/2 were activated by LDL, only p38 is responsible for the LDL effects, as evidenced by a complete blockade by SB203580. Moreover, pretreatment with catalase significantly decreased the extent of IL-8 up-regulation but pretreatment with diphenylene iodinium, N-acetylcysteine, or polyethylene glycol-conjugated superoxide dismutase caused a mild decrease. Activation of activator protein(AP)-1 by p38 appears to be necessary along with the concomitant up-regulation of c-fos and c-Jun. In addition, participation of nuclear factor(NF)-kB was also found to be essential for the LDL response, as judged by EMSA and luciferase reporter assay. In summary, native LDL stimulated IL-8 expression is conveyed via PTX-sensitive Gi receptors, the generation of H₂O₂, the phosphorylation of p38 MAPK, and the concerted action of AP-1 and NF-kB. The IL-8 has autocrine effect on hAoSMC's migration and proliferation, and is contributable phenomena of VSMC in atherogenesis. Human aortic smooth muscle cells(hAoSMCs) appear to playa key role in the initiation and progression of atherosclerosis and restenosis via the up-regulation of interleukin(IL)-8 under hyperlipidemic conditions. In addition, the signaling pathway of native LDL-induced VSMC proliferation and the relationship with PPARs will be discussed.
인간 리포코틴 - 1 유전자의 클로닝 및 대장균에서의 발현
허광래,박순희,강성만,송인성,이혜영,나도선 ( Kwahng Rae Huh,Soon Hee Park,Sung Man Kang,In Sung Song,Hay Young Lee,Doe Sun Na ) 생화학분자생물학회 1990 BMB Reports Vol.23 No.4
A cDNA clone coding for lipocortin-1 was isolated from the cDNA library of human placental mRNA. Plasmid pHT1 was constructed by inserting the coding sequence into plasmid pKK233-2, a universal expression vector containing trc promoter. Lipocortin-1 was expressed constitutively or by induction with IPTG in E. colt strain C600 or JM109 harboring pHT1. The activity of purified lipocortin-1 was demonstrated by the in vitro phospholipase A₂ inhibitory activity.
허광래 ( Kwang-lae Hoe ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
국가의 연구 전략 및 정책을 이해하는 것은 각자의 연구비를 확보하여 원할한 연구를 수행하는데 중요하다. 우리나라의 대부 분의 연구비는 국책연구비 이므로 국가 R&D 시스템을 이해하는 것은 연구자의 연구비 안정화에도 중요한 부분을 차지한다. 하지만 대부분의 연구자가 기초와 국책의 정의에서부터 이해도가 부족하며, 국가 연구비가 어떠한 과정으로 진행되는지 모르 고 있는 실정이다. 그러므로 국가 연구비에서 바이오가 차지하는 비중과 연구내용을 파악하는 것도 본인의 연구방향 설정에 중요한 부분이 될 수 있다. 국가 R&D 시스템의 경우 등장인물이 많으며 각자의 역할도 복잡하며, 각 정부 부처의 역할이 이중 삼중으로 레이어를 이루고 있으므로, 어떠한 과정으로 연구비 배정 전략과 정책이 작용하는지 이해하는 것이 필요하다. 특히 연구자들이 알 수 없는 많은 법과 계획 및 민간위원회가 존재하고 있다는 것을 이해하는 것이 중요하다. 본 세미나를 통하여 연구자가 국가의 연구비 정책을 좀 더 잘 이해하는 것은 본인의 연구비 확보에도 중요하지만 국가가 연구 정책을 세울 때 올바른 현장의 목소리를 내는 것에도 중요하다.
COVID-19 팬데믹이 국가R&D 연구성과 창출 비용에 미친 영향 - 기초연구사업 SCI논문 성과를 중심으로 -
차윤경,허광래,이홍석 한국콘텐츠학회 2023 한국콘텐츠학회논문지 Vol.23 No.11
This study examined the impact of the COVID-19 pandemic on the research achievement costs of SCI papers by academic disciplines, focusing on the basic research program of the Ministry of Science and ICT. Based on precedent studies, COVID-19 had a negative impact not only on academia but on society as a whole. In this respect, this study hypothesized that the research costs per SCI paper for basic research program would increase following the outbreak of COVID-19. More specifically, the study hypothesized and sought to confirm that the field of medical sciences were most affected by COVID-19 due to social distancing measures and economic recession, as it is a field that demands high research costs, such as material costs, and requires research to be conducted in laboratories. The results of this study may be used as a basis for establishing national R&D policies in response to future pandemics.
박일환,황혜미,전병화,권형주,허광래,김영명,유승우 생화학분자생물학회 2015 Experimental and molecular medicine Vol.47 No.-
Elevated plasma concentration of native low-density lipoprotein (nLDL) is associated with vascular smooth muscle cell (VSMC) activation and cardiovascular disease. We investigated the mechanisms of superoxide generation and its contribution to pathophysiological cell proliferation in response to nLDL stimulation. Lucigenin-induced chemiluminescence was used to measure nLDL-induced superoxide production in human aortic smooth muscle cells (hAoSMCs). Superoxide production was increased by nicotinamide adenine dinucleotide phosphate (NADPH) and decreased by NADPH oxidase inhibitors in nLDL-stimulated hAoSMC and hAoSMC homogenates, as well as in prepared membrane fractions. Extracellular signal-regulated kinase 1/2 (Erk1/2), protein kinase C-θ (PKCθ) and protein kinase C-β (PKCβ) were phosphorylated and maximally activated within 3 min of nLDL stimulation. Phosphorylated Erk1/2 mitogen-activated protein kinase, PKCθ and PKCβ stimulated interactions between p47phox and p22phox; these interactions were prevented by MEK and PKC inhibitors (PD98059 and calphostin C, respectively). These inhibitors decreased nLDL-dependent superoxide production and blocked translocation of p47phox to the membrane, as shown by epifluorescence imaging and cellular fractionation experiments. Proliferation assays showed that a small interfering RNA against p47phox, as well as superoxide scavenger and NADPH oxidase inhibitors, blocked nLDL-induced hAoSMC proliferation. The nLDL stimulation in deendothelialized aortic rings from C57BL/6J mice increased dihydroethidine fluorescence and induced p47phox translocation that was blocked by PD98059 or calphostin C. Isolated aortic SMCs from p47phox− / − mice (mAoSMCs) did not respond to nLDL stimulation. Furthermore, NADPH oxidase 1 (Nox1) was responsible for superoxide generation and cell proliferation in nLDL-stimulated hAoSMCs. These data demonstrated that NADPH oxidase activation contributed to cell proliferation in nLDL-stimulated hAoSMCs.
h-Prune as a novel binding protein of NS5A that regulates ERK1/2 activation
남미영,김철희,김동욱,이숙정,허광래 한국응용생명화학회 2016 Applied Biological Chemistry (Appl Biol Chem) Vol.59 No.4
Hepatitis C virus (HCV) non-structural 5A (NS5A) protein is associated with a wide variety of host signaling pathways by binding to C-terminal polyproline (PxxP) motifs of various proteins. In this study, we used yeast two-hybrid analysis and a GST pull-down assay to screen a novel NS5A interacting protein and elucidate the binding site and cellular signaling by focusing on recombinant human epidermal growth factor (rhEGF)-mediated ERK1/2 activation. Screening a liver cDNA library revealed that h-prune, a member of the DHH (Asp-His-His) protein superfamily, directly interacted with HCV NS5A C-terminus. In particular, a mutation of five proline amino acids to alanine in this region revealed that these two proteins produced strong interaction through this domain. It is known that h-prune possesses a highly conserved DHH motif, which has exopolyphosphatase activity that accelerates hydrolysis of inorganic polyphosphate. A timechasing analysis after rhEGF treatment demonstrated that h-prune overexpression almost restored NS5A-mediated attenuation of ERK1/2 phosphorylation, but h-prune itself did not alter this signaling. Although the detailed mechanisms need to be clarified, this study demonstrates that h-prune interacts directly with the PxxP motif of the HCV NS5A C-terminus and that this binding alters the rhEGF-mediated ERK1/2 signaling cascade in liver cells.