• Nuclear Engineering and Technology
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• v.42 no.5
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• pp.562-567
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• 2010

A One-Dimensional Water Flow and Contaminant Transport in Unsaturated Zone (FTUNS) code has been developed in order to interpret radionuclide migration in an unsaturated zone. The pore-size distribution index (n) and the inverse of the air-entry value ($\alpha$) for an unsaturated zone were measured by KS M ISO 11275 method. The hydraulic parameters of the unsaturated soil are investigated by using soil from around a nuclear facility in Korea. The effect of hydraulic parameters on radionuclide migration in an unsaturated zone has been analyzed. The higher the value of the n-factor, the more the cobalt concentration was condensed. The larger the value of $\alpha$-factor, the faster the migration of cobalt was and the more aggregative the cobalt concentration was. Also, it was found that an effect on contaminant migration due to the pore-size distribution index (n) and the inverse of the air-entry value ($\alpha$) was minute. Meanwhile, migrations of cobalt and cesium are in inverse proportion to the Freundich isotherm coefficient. That is to say, the migration velocity of cobalt was about 8.35 times that of cesium. It was conclusively demonstrated that the Freundich isotherm coefficient was the most important factor for contaminant migration.

• Journal of Life Science
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• v.26 no.10
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• pp.1189-1195
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• 2016

Vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are potent angiogenic factors that have been used clinically to induce angiogenesis. To enable migration and invasion, cells must proliferate and secrete proteinases, which degrade the surrounding extracellular matrix. The goal of this study was to investigate the cell proliferation; matrix metalloproteinase-2 (MMP-2), MMP-9, and plasmin secretion; and migration and invasion of glioma-derived U-373-MG cells induced by VEGF and HGF treatment. An additional goal was to test the hypothesis that elevated secretion of MMP-2, MMP-9, and plasmin contributed directly or indirectly to the proliferation, migration, and invasion of U-373-MG cells. Cell proliferation, migration, and invasion and MMP-2, MMP-9, and plasmin secretion were significantly increased in the VEGF and HGF-treated U-373-MG cells. To elucidate the role of the increased secretion of MMP-2, MMP-9, and plasmin in cell proliferation, migration, and invasion of the U-373-MG cells, they were treated with MMPs inhibitor (BB-94) and plasmin inhibitor (α2AP) prior to VEGF or HGF stimulation. The BB-94 and α2AP treatment resulted in a significant reduction in the cell proliferation, migration, and invasion of the U-373-MG cells as compared with the VEGF- and HGF-treated groups. The results indicate that inhibition of MMPs and plasmin reduce the cell proliferation, migration, and invasion of U-373-MG cells.

• BMB Reports
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• v.53 no.12
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• pp.646-651
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• 2020

Bone resorption is linked to bone formation via temporal and spatial coupling within the remodeling cycle. Several lines of evidence point to the critical role of coupling factors derived from pre-osteoclasts (POCs) during the regulation of bone marrow-derived mesenchymal stem cells (BMMSCs). However, the role of glial cell-derived neurotrophic factor (GDNF) in BMMSCs is not completely understood. Herein, we demonstrate the role of POC-derived GDNF in regulating the migration and osteogenic differentiation of BMMSCs. RNA sequencing revealed GDNF upregulation in POCs compared with monocytes/macrophages. Specifically, BMMSC migration was inhibited by a neutralizing antibody against GDNF in pre-osteoclast-conditioned medium (POC-CM), whereas treatment with a recombinant GDNF enhanced migration and osteogenic differentiation. In addition, POC-CM derived from GDNF knock-downed bone marrow macrophages suppressed BMMSC migration and osteogenic differentiation. SPP86, a small molecule inhibitor, inhibits BMMSC migration and osteogenic differentiation by targeting the receptor tyrosine kinase RET, which is recruited by GDNF into the GFRα1 complex. Overall, this study highlights the role of POC-derived GDNF in BMMSC migration and osteogenic differentiation, suggesting that GDNF regulates bone metabolism.

• Asia-Pacific Journal of Business Venturing and Entrepreneurship
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• v.12 no.5
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• pp.39-53
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• 2017

The purpose of this study was to investigate the effects of the rural migration factors, degree of preparation for migration, lifestyle conditions and support policies reflected against the family satisfaction of the migration. In this study family factors were used as control variables. Independent variables for this study will consist of the factors of rural migration, the degree of preparation for migration, living conditions of the farmers and the support policies, where as the dependent variable is the satisfaction of migration with an adjusting factor of the family satisfaction which will be further analysed to identify its effects on the dependent variable. For this study, a questionnaire survey was conducted for the residents and 237 valid questionnaires were collected. Multiple regression analysis was performed based on the collected data where demographic attributes being the controlling variable, and regression analysis was performed for the adjusting variable of the family. As the economic factor increases, the level of satisfaction generated to be higher in rural migration. As for the degree of preparation, living condition and support policies resulted, great quantity of green nature, safety and agriculture startup support, respectively, indicated a positive effect to the satisfaction level of migration. From the results, adjustment effect of the family factors on the economic, nature, convenience and satisfaction of the migration have appeared. The conclusion of this study is that policy support, regional stability, and economic gain are the most important factors to increase satisfaction and to reduce re-migration rate to city.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.326.2-327
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• 2002

Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival and differentiation. In this study, we examined the effect of GDNF on proliferation and migration of Hs683 human glioma cells. GDNF markedly enhances proliferation and migration of Hs683 cells in a dose-dependent manner. (omitted)

• Proceedings of the Korean Society of Applied Pharmacology
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• 2003.11a
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• pp.76-76
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• 2003

Mast cells accumulation can be causally related with several allergic inflammations. Previous work has demonstrated that glucocorticoids decreased tissue mast cell number and stem cell factor (SCF)-induced migration of mast cells required p38 mitogen-activated protein kinase (MAPK) activation. In the present study, we investigated the effects of dexamethasone on SCF-induced migration of rat peritoneal mast cells (RPMCs). SCF significantly induced migration of RPMCs at 4 h. Dexamethasone dose-dependently inhibited SCF-induced migration of RPMCs (about 90.1% at 100 nM, P<0.05). MAPK p38 inhibitor, SB203580 (20 ${\mu}$M) also inhibited the SCF-induced migration. The ability of SCF to enhance morphological alteration and F -actin formation was also abolished by treatment of dexamethasone. Dexamethasone inhibited SCF-induced p38 MAPK activation to near basal level and induced the MKP-1 expression. In addition, SCF-induced inflammatory cytokine production was significantly inhibited by treatment of dexamethasone or SB203580 (p<0.01). Our results show that dexamethasone potently regulates SCF -induced migration, p38 MAPK activation and inflammatory cytokine production through expression of MKP-l protein in RPMCs. Such modulation may have functional consequences during dexamethasone treatment, especially mast cell-mediated allergic inflammation disorders.

• Journal of Veterinary Clinics
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• v.38 no.6
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• pp.261-268
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• 2021

The study was conducted to evaluate the effects of carboxymethyl chitosan (CMC) on proliferation, migration, and lipopolysaccharide (LPS)-induced inflammatory response in canine bone marrow-derived mesenchymal stem cells (BMSCs). The proliferation and migration of BMSCs were examined after treatment with CMC. The effect of CMC on the mRNA expression of inflammatory cytokines, such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β, was also evaluated by reverse transcription polymerase chain reaction (RT-PCR). In the proliferation assay, no significant changes were found at all CMC concentrations compared with controls. The migration assay showed that CMC dose-dependently stimulated the migration of BMSCs in normal and LPS-treated conditions. RT-PCR showed that TNF-α and IL-10 expressions were suppressed in the BMSCs after CMC treatment. However, other genes were not affected. Taken together, CMC promoted BMSC migration and inhibited TNF-α and IL-10. Therefore, CMC may be possible to regulate wound healing when mesenchymal stem cells are applied in inflammatory diseases.

• International Journal of Oral Biology
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• v.43 no.3
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• pp.161-169
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• 2018

We previously demonstrated that epidermal growth factor (EGF) enhances cell migration and invasion of breast cancer cells in a SMAD ubiquitination regulatory factor 1 (SMURF1)-dependent manner and that SMURF1 induces degradation of ${\beta}-catenin$ in C2C12 cells. However, the relationship between EGF-induced SMURF1 and ${\beta}-catenin$ expression in breast cancer cells remains unclear. So, we investigated if EGF and SMURF1 regulate ${\beta}-catenin$ expression in MDAMB231 human breast cancer cells. When MDAMB231 cells were incubated with EGF for 24, 48, and 72 hours, EGF significantly increased expression levels of SMURF1 mRNA and protein while suppressing expression levels of ${\beta}-catenin$ mRNA and protein. Overexpression of SMURF1 downregulated ${\beta}-catenin$ mRNA and protein, whereas knockdown of SMURF1 increased ${\beta}-catenin$ expression and blocked EGF-induced ${\beta}-catenin$ downregulation. Knockdown of ${\beta}-catenin$ enhanced cell migration and invasion of MDAMB231 cells, while ${\beta}-catenin$ overexpression suppressed EGF-induced cell migration and invasion. Furthermore, knockdown of ${\beta}-catenin$ enhanced vimentin expression and decreased cytokeratin expression, whereas ${\beta}-catenin$ overexpression decreased vimentin expression and increased cytokeratin expression. These results suggest that EGF downregulates ${\beta}-catenin$ in a SMURF1-dependent manner and that ${\beta}-catenin$ downregulation contributes to EGF-induced cell migration and invasion in MDAMB breast cancer cells.

• KSBB Journal
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• v.18 no.6
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• pp.485-489
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• 2003

Hepatocyte growth factor (HGF) is a mesenchymal-derived cytokine. It exerts a motogenic effect on various target cells, which is displayed either by cell scattering, locomotion, and migration during the wound repair process of cultured cells, or invasiveness through the extracellular matrix, in vitro. Although it is known that HGF influences the motogenic effect of endothelial cells, the precise effects of HGF during migration are still poorly understood. To elucidate the role of HGF in endothelial cell migration, the effect of HGF on endothelial cell migration and MMPs and plasmin production were studied. We found that HGF induces the migration of cultured endothelial cells through increased MMPs and plasmin secretion.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.405-413
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• 2020

Fibroblast-like synoviocytes (FLS) play a crucial role in initiating rheumatoid arthritis. B-cell activating factor (BAFF) plays a role in FLS survival as well as in B cell maturation and maintenance. Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls FLS migration and whether BAFF expression in FLS could be regulated by KR33426 which is the inhibitor of BAFF binding to BAFF receptors (BAFF-R) by using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells migrated compared to the control. TNF-α increased BAFF expression in FLS, significantly. FLS migration was inhibited by the transfection with BAFF-siRNA. KR33426 also inhibited BAFF expression increased by TNF-α treatment in FLS as judged by western blotting, PCR, and transcriptional activity assay. Kinases including JNK, p38 and Erk were activated by TNF-α treatment. While JNK and p38 were inhibited by KR33426 treatment, no changes in Erk were observed. Transcription factors including p65, c-Fos, CREB and SP1 were enhanced by TNF-α treatment. Among them, c-Fos was inhibited by KR33426 treatment. Small interference(si)-RNA of c-fos decreased BAFF transcriptional activity. FLS migration induced by TNF-α was inhibited by the transfection with BAFF-siRNA. KR33426 increased Twist, Snail, Cadherin-11 and N-Cadherin. In contrast, KR33426 decreased E-cadherin and TNF-α-enhanced CCL2. Taken together, our results demonstrate that synovial cell migration via CCL2 expression could be regulated by BAFF expression which is decreased by KR33426 and c-Fos-siRNA. It suggests for the first time that the role of BAFF-siRNA on FLS migration might be matched in the effect of KR33426 on BAFF expression.