• Journal of Periodontal and Implant Science
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• v.29 no.4
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• pp.803-823
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• 1999

In order to reveal immunopathogenesis of periodontal tissue destruction, it is important to clarify the molecular mechanism of trafficking and retention of activated leukocytes, including monocytes/macrophages. Gingival fibroblasts may be involved in the regulation of inflammatory cell accumulation in the extravascular periodontal connective tissues via cytokine production and surface expression of adhesion molecules. In this study, it was investigated the molecular basis for the adhesive interactions between monocytes and fibroblasts such as peri-odontal ligament fibroblast(PDLF), human gingival fibroblast(HGF), and human dermal fibroblast(HDF). First, it was examined the evidence whether monocyte-fibroblast cell contact may cause signal transduction in fibroblasts. Being directly in contact with fixed human monocyte cell line THP-1, or U937, upregulation of IL-6 production, $TNF-{\alpha}$ mRNA expression and increased cell proliferation could be seen for fibroblasts. IL-6 production induced by monocyte- fibroblast coculture were further increased when fibroblasts had been pretreated with $IFN-{\gamma}$ or $IL-1{\beta}$ , and monocytes with LPS. Next, it was examined the expression of ICAM-1 which has been known to be involved in accumulation and activation of leukocytes in inflammatory diseases such as periodontitis. ICAM-1 was upregulated up to 10-fold on PDLF, HGF, and HDF by exposure to $IFN-{\gamma}$ or $IL-1{\beta}$. Furthermore, anti-ICAM-1 monoclonal antibody clearly blocked cocultureinduced IL-6 production by fibroblasts, suggesting that $ICAM-1/{\beta}_2$integrin pathway is involved in periodontal fibroblastmonocyte interaction. Overall, these findings provide evidence that periodontal fibroblasts could be involved in the accumulation and retention of monocytes/macrophages in periodontal inflammatory lesion at least in part by ICAM-1 expression. In addition, periodontal fibroblast-monocyte interaction could cause activation signals in fibroblasts intracellularly which result in cytokine production and cell proliferation. Thus, periodontal fibroblasts are speculated to play an important role in immunoregulation and tissue destruction in chronic periodontal diseases by interaction with monocytes/macrophages.

• Journal of the Korean Regional Science Association
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• v.15 no.2
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• pp.155-187
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• 1999

The East Asian Region has experienced remarkable economic growth and transformation of interurban networking over the past three decades, and urban competiti veness for a networking hub in this region has become a critical issue confronting cities. Competitiveness of the Seoul capital region for a networking hub in Northeast Asia is outstripped by other competing cities in East Asia, notwithstanding its geo-politically and geo-economically advantageous location in this region. In this paper, we aim to appraise the Seoul capital region's competitiveness in terms of logistics distribution, financial function and logistics distribution, financial function and agglomeration of transnational corporations (especially of RHOs and other managerial functions), and to advance the networking strategies of the region for a Northeast Asia hyb. As a result of analysis, we suggest that the Seoul capital region be developed as a Northeast Asian center for regional headquarters or leading global corporations and financial services for being a strategic nodal point in Northeast Asia in the 21st century. A recent survey shows that where to locate an RHQ is influenced by various factors, such as potential market and manufacturing site in the city's hinterland, quality of life, such things as culture, health, safety, education, a well-educated, English-speaking population, reliable air transport, state-of-the-art communications, and an active policy to offer foreign companies generous incentives. The Seoul capital region, which is located at a strategic nodal point advantageous as a springboard for its Northeast Asian hinterland, cannot meet the other conditions mentioned above. To overcome these drawbacks in attracting transnational capital and to create competitiveness as a strategic hub of RHQs in Northeast Asia, it is urgent to initiate a structural reform of the Korean economy, politics, and overall society, to minimize the regulation of FDI, and to provide various incentives for foreign investment. Moreover, we propose the construction of an 'International Business Town' in the Seoul capital region, as a medium to intermediate these strategies and to shape them in a spatial scale. The projected 'International Business Town(IBT)' will be a 'free city' open to international business in which liberal economic activities are guaranteed by special legislation and administration, infrastructures needed for international and improved accessibility to the airport are furnished, and the preference of foreign high-income investors for cultural and living environment are satisfactorily met. IBT is conspicuously differentiated from a raft of other cities' incentives in that it combines deregulation and incentive programs to attract the investment of transnational capital, with a spatial program of offering an urban environment preferred by the high-income investors for cultural and living environment are satisfactorily met. IBT is conspicuously differentiated from a raft of other cities' incentives in that it combines deregulation and incentive programs to attract the investment of transnational capita, with a spatial program of offering an urban environment preferred by the high-income and managerial class. Furthermore, it can be an excellent way of overcoming the xenophobia that has spread among the Korean population by concentrating foreign businesses and their lifestyles in a specific foreign businesses and their lifestyles in a specific zone. In conclusion, 'International Business Town', in line with other legislative and administrative incentive programs, will function as a driving force to make the Seoul capital regional more competitive as a regional business hub in Northeast Asia.

• Radiation Oncology Journal
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• v.17 no.3
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• pp.223-229
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• 1999

Purpose : The expression pattern of c-jun by ionizing radiation according to cell growth state (exponential growth vs. stationary phase) and its relationship with cell cycle redistribution were investigated. Materials and Methods : The exponential growth phase (day 4) and stationary phase (day 9) cells were determined from cell growth curve according to the elapse of days in CaSki. The cells were irradiated using 6 MV X-ray with a dose of 2 Gy at a fixed dose rate of 3 Gy/min. Northern blot analysis was peformed with total cellular RNA and cell cycle distribution was analyzed using flow cytometry according to time-course after irradiation. Results : The maximum expression of c-jun occurred 1 hour after irradiation in both exponential growth and stationary phase cells. After then c-jun expression was elevated upto 6 hours in exponential growth phase cells, but the level decreased in stationary phase cells. Movements of cells from G0-G1 to S, G2-M phase after irradiation were higher in exponential growth phase than stationary phase. Conclusion : c-jun may be involved in the regulation of cellular proliferation according to the growth states after irradiation.

• Journal of Life Science
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• v.21 no.7
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• pp.923-931
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• 2011

In the present study, we investigated the effect of indole-3-carbinol (I3C), a natural compound present in vegetables, on the cell migration and invasion of OVCAR-3 ovarian cancer cells. Our results indicated that I3C inhibited the proliferation of OVCAR-3 cells, a process which was associated with inhibition of cell motility as determined by wound healing experiments and cell invasion studies. I3C treatment increased the tightness of the tight junctions (TJs), which was demonstrated by an increase in transepithelial electrical resistance and a decrease in paracellular permeability. The RT-PCR and immunoblotting results indicated that I3C repressed the levels of claudin-3 as well as claudin-4, proteins that comprise a major part of TJs and play a key role in the control and selectivity of paracellular transport. Furthermore, the activities of matrix metalloproteinase (MMP)-2 and MMP-9 were also decreased by treatment with I3C, which was connected with the down-regulation of their mRNAs and protein expression. The results suggest that I3C may be expected to inhibit cancer cell metastasis and invasion by restoring TJs and decreasing MMP activity in ovarian cancer cell line OVCAR-3.

• Asian-Australasian Journal of Animal Sciences
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• v.31 no.8
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• pp.1366-1372
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• 2018

Objective: A disintegrin and metallopeptidase with thrombospondin motifs type 8 (ADAMTS8) is crucial for diverse physiological processes, such as inflammation, tissue morphogenesis, and tumorigenesis. The chicken ADAMTS8 (chADAMTS8) gene was differentially expressed in the kidney following exposure to different calcium concentrations, suggesting a pathological role of this protein in metabolic diseases. We aimed to examine the molecular characteristics of chADAMTS8 and analyze the gene-expression differences in response to toll-like receptor 3 (TLR3) stimulation. Methods: The ADAMTS8 mRNA and amino acid sequences of various species (chicken, duck, cow, mouse, rat, human, chimpanzee, pig, and horse) were retrieved from the Ensembl database and subjected to bioinformatics analyses. Reverse-transcription polymerase chain reaction (RT-PCR) and quantitative PCR (qPCR) experiments were performed with various chicken tissues and the chicken fibroblast DF-1 cell line, which was stimulated with polyinosinic-polycytidylic acid (poly[I:C]; a TLR3 ligand). Results: The chADAMTS8 gene was predicted to contain three thrombospondin type 1 (TSP1) domains, whose amino acid sequences shared homology among the different species, whereas sequences outside the TSP1 domains (especially the amino-terminal region) were very dif­ferent. Phylogenetic analysis revealed that chADAMTS8 is evolutionarily clustered in the same clade with that of the duck. chADAMTS8 mRNA was broadly expressed in chicken tissues, and the expression was significantly up-regulated in the DF-1 cells in response to poly(I:C) stimulation (p<0.05). These results showed that chADAMTS8 may be a target gene for TLR3 signaling. Conclusion: In this report, the genetic information of chADAMTS8 gene, its expression in chicken tissues, and chicken DF-1 cells under the stimulation of TLR3 were shown. The result suggests that chADAMTS8 expression may be induced by viral infection and correlated with TLR3-mediated signaling pathway. Further study of the function of chADAMTS8 during TLR3-dependent inflammation (which represents RNA viral infection) is needed and it will also be important to examine the molecular mechanisms during different regulation, depending on innate immune receptor activation.

• Journal of Life Science
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• v.24 no.8
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• pp.837-842
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• 2014

The purpose of this study was to investigate the effect of Brunfelsia grandiflora ethanol extract (BGEE) on the induction of autophagy via regulation of SIRT1 expression and p53 activation in a human lung fibroblast cell line, IMR 90. BGEE at a concentration of $5{\mu}g/ml$ or more exhibited a cytotoxic effect on IMR 90 cells. For the first time, this study showed that BGEE induces autophagy in normal human lung fibroblasts. BGEE also increased the expression level of beclin-1 at $2.5{\mu}g/ml$ or less and Atg7 at $5{\mu}g/ml$, both of which are known to be involved in the induction of autophagy. In addition, BGEE modulated the expression of other proteins related to autophagy in normal human lung fibroblasts. The expression levels of p53 and p-p53, an active form of p53, were decreased in the presence of BGEE at a noncytotoxic concentration. In contrast, the expression level of SIRT1 was increased in human lung fibroblasts treated with BGEE at a noncytotoxic concentration. Moreover, SA-${\beta}$-Gal staining, an aging marker, was reduced in the normal human lung fibroblasts treated with BGEE. These findings suggest that BGEE promotes the induction of autophagy and antiaging through the modulation of p53 and SIRT1 in human lung fibroblasts.

• Journal of Life Science
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• v.30 no.11
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• pp.973-982
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• 2020

In this study, we examined inhibition of adipocyte differentiation associated with the administration of camphor, a substance identified in extracts of the flowering plant Chrysanthemum indicum L. (CI). No camphor-mediated cytotoxicity was observed over a period of 1-10 days in studies targeting cells of the 3T3-L1 adipocyte-like line. Experiments that featured siRNA-mediated suppression of the transmembrane proteins Patched (PTCH) and Smoothened (SMO) resulted in inhibition and activation of differentiation, respectively. Interestingly, inhibition of PTCH typically activates SMO protein targeting and serves to activate hedgehog (HH)-mediated signaling. The results of our study suggest that activation of HH-mediated signaling can inhibit adipocyte differentiation. Furthermore, expression of glioma-associated oncogene homologue 1 (Gli1) was detected by flow cytometry in 62.7±1.5% of cells in response to administration of Lactobacillus rhamnosus (KCTC 3237) and in 60.4±2.2% of cells in response to camphor; these levels are higher than those detected in undifferentiated controls (24.9±3.1%). No change in the state of fermented camphor was identified by gas chromatography-mass spectrometry (GC-MS), but a 15.41% quantitative increase was confirmed in KCTC 3237. Overall, we conclude that administration of camphor resulted in overexpression of SMO and modulated the differential expression of Gli1. Animal studies focused on the impact of camphor as an agent to counteract obesity might be considered in the future. Indeed, camphor and similar physiologically active compounds from fermented CI might be developed as new and effective treatments for obesity.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.3
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• pp.219-228
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• 2015

Excessive microglial activation and subsequent neuroinflammation lead to synaptic loss and dysfunction as well as neuronal cell death, which are involved in the pathogenesis and progression of several neurodegenerative diseases. Thus, the regulation of microglial activation has been evaluated as effective therapeutic strategies. Although dieckol (DEK), one of the phlorotannins isolated from marine brown alga Ecklonia cava, has been previously reported to inhibit microglial activation, the molecular mechanism is still unclear. Therefore, we investigated here molecular mechanism of DEK via extracellular signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, $1{\mu}g/ml$)-stimulated BV-2 microglia. In addition, DEK markedly attenuated Akt phosphorylation and increased expression of $gp91^{phox}$, which is the catalytic component of NADPH oxidase complex responsible for microglial reactive oxygen species (ROS) generation. Finally, DEK significantly attenuated neuronal cell death that is induced by treatment of microglial conditioned media containing neurotoxic secretary molecules. These neuroprotective effects of DEK were also confirmed in a neuron-microglia co-culture system using enhanced green fluorescent protein (EGFP)-transfected B35 neuroblastoma cell line. Taken together, these results suggest that DEK suppresses excessive microglial activation and microglia-mediated neuronal cell death via downregulation of ERK, Akt and NADPH oxidase-mediated pathways.

• Tuberculosis and Respiratory Diseases
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• v.63 no.2
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• pp.145-153
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• 2007

Background: Asthma is a syndrome that is characterized by a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Colchicine is an inexpensive and safe medication with unique anti-inflammatory properties. IL-1Ra (Interleukin-1 receptor antagonist) mediates the anti-inflammatory effect in human inflammatory diseases, including asthma. This study examined whether IL-1Ra mediates the anti-inflammatory effect of colchicine in normal human bronchial epithelial cells (NHBE), RAW 264.7 cells (murine macrophage cell line), and a mouse lung. Methods: NHBE, RAW 264.7 cells and BALB/c mice were stimulated with colchicine, and the increase in the IL-1Ra level was estimated by ELISA, Western analysis and RT-PCR analysis. Results: Colchicine stimulated NHBE and RAW 264.7 cells to release IL-1Ra into the supernatant in a dose-and time-dependent manner. The major isoform of IL-1Ra in NHBE and RAW 264.7 cells is type I icIL-1Ra, and sIL-1Ra, respectively. IL-1Ra up-regulation was blocked by PD98059, a specific inhibitor in MAPK pathways. Colchicine also stimulated the secretion of IL-1Ra into the bronchoalveolar lavage (BAL) fluid of BALB/c mouse. Conclusion: Colchicine stimulates an increase in the IL-1Ra level both in vivo and in vitro, and might have an anti-inflammatory effect.

• Journal of Periodontal and Implant Science
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• v.36 no.2
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• pp.385-396
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• 2006

For the regeneration of periodontal tissues, the microenvironment for new attachment of connective tissue fibers should be provided, At this point of view, cementum formation in root surface plays a key role for this new attachment. This study was performed to figure out which factor promotes differentiation of cementoblast Considering anatomical structure of tooth, we selected the cells which may affect the differentiation of cementoblast - Ameloblast, OD11&MDPC23 for odontoblasts, NIH3T3 for fibroblsts and MG63 for osteoblasts. And OCCM30 was selected for cementoblast cell line. Then, the cell lines were cultured respectively and transferred the conditioned media to OCCM30. To evaluate the result, Alizarin red S stain was proceeded for evaluation of mineralization. The subjected mRNA genes are bone sialoprotein(BSP), alkaline phosphate(ALP) , osteocalcin(OC), type I collagen(Col I), osteonectin(SPARC ; secreted protein acidic and rich in cysteine). Expression of the gene were analysed by RT-PCR, The results were as follows: 1. For alizarin red S staining, control OCCM30 didn't show any mineralized red nodules until 14 days. But red nodules started to appear from about 4 days in MDPC-OCCM30 & OD11-OCCM30. 2. For results of RT-PCR, ESP mRNAs of control-OCCM30 and others were expressed from 14 days, but in MDPC23-OCCM30 & OD11-OCCM30 from 4 days. Like this, the gene expression of MDPC23-OCCM30 & OD11-OCCM30 were detected much earlier than others. 3. For confirmation of odontoblast effect on cementoblast, conditioned media of osteoblasts(MG63) which is mineralized by producing matrix vesicles didn't affect on the mineralized nodule formation of cementoblasts(OCCM30). This suggest the possibility that cementoblast mineralization is regulated by specific factor in dentin matrix protein rather than matrix vesicles. Therefore, we proved that the dentin/odontoblast promotes differentiation/mineralization of cementoblasts. This new approach might hole promise as diverse possibilities for the regeneration of tissues after periodontal disease.