• Journal of Life Science
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• v.26 no.12
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• pp.1367-1375
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• 2016

Cilostazol is known to be a selective inhibitor of phosphodiesterase III and is generally used to treat stroke. Our previous findings showed that cilostazol enhanced capillary density through angiogenesis after focal cerebral ischemia. Angiogenesis is an important physiological process for promoting revascularization to overcome tissue ischemia. It is a multistep process consisting of endothelial cell proliferation, migration, and tubular structure formation. Here, we examined the modulatory effect of cilostazol at each step of the angiogenic mechanism by using human brain microvascular endothelial cells (HBMECs). We found that cilostazol increased the migration of HBMECs in a dose-dependent manner. However, it did not enhance HBMEC proliferation and capillary-like tube formation. We used a cDNA microarray to analyze the mechanisms of cilostazol in cell migration. We picked five candidate genes that were potentially related to cell migration, and we confirmed the gene expression levels by real-time PCR. The genes phosphoserine aminotransferase 1 (PSAT1) and CCAAT/enhancer binding protein ${\beta}$ ($C/EBP{\beta}$) were up-regulated. The genes tissue factor pathway inhibitor 2 (TFPI2), retinoic acid receptor responder 1 (RARRES1), and RARRES3 were down-regulated. Our observations suggest that cilostazol can promote angiogenesis by promoting endothelial migration. Understanding the cilostazol-modulated regulatory mechanisms in brain endothelial cells may help stimulate blood vessel formation for the treatment of ischemic diseases.

• Journal of Life Science
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• v.28 no.12
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• pp.1516-1522
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• 2018

Atherosclerosis is an obstructive vessel disease mainly caused by chronic arterial inflammation to which the proliferation and migration of vascular smooth muscle cells (VSMCs) is the main pathological response. In the present study, the primary responsible inflammatory cytokine and its signaling pathway was investigated. The proliferation and migration of VSMCs was significantly enhanced by the prostaglandin $F_{2{\alpha}}$ ($PGF_{2{\alpha}}$), while neither was affected by tumor necrosis factor ${\alpha}$. Prostacyclin $I_2$ was seen to enhance the proliferation of VSMCs while simultaneously suppressing their migration. Both prostaglandin $D_2$ and prostaglandin $E_2$ significantly enhanced the migration of VSMCs, however, proliferation was not affected by either of them. The proliferation and migration of VSMCs stimulated by $PGF_{2{\alpha}}$ progressed in a dose-dependent manner; the $EC_{50}$ value of both proliferation and migration was $0.1{\mu}M$. VSMCs highly expressed the phospholipase isoform $C-{\beta}3$ ($PLC-{\beta}3$) while others such as $PLC-{\beta}1$, $PLC-{\beta}2$, and $PLC-{\beta}4$ were not expressed. Inhibition of the PLCs by U73122 completely blocked the $PGF_{2{\alpha}}$-induced migration of VSMCs, and, in addition, silencing $PLC-{\beta}3$ significantly diminished the $PGF_{2{\alpha}}$-induced proliferation and migration of VSMCs. Given these results, we suggest that $PGF_{2{\alpha}}$ plays a crucial role in the proliferation and migration of VSMCs, and activation of $PLC-{\beta}3$ could be involved in their $PGF_{2{\alpha}}$-dependent migration.

• Journal of the Korean Orthopaedic Association
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• v.54 no.3
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• pp.237-243
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• 2019

Purpose: To analyze the risk factors for posterior migration of a single cage after transforminal lumbar interbody fusion (TLIF). Materials and Methods: This study was conducted retrospectively on 48 patients (60 discs) who were followed-up for 1 year after TLIF from January 2015 to January 2017. The patients were divided into two groups: group 1 containing 16 patients (17 discs) with cage migration and group 2 containing 32 patients (43 discs) without it. Information related to cage migration, such as the demographic factors, shape of disc, level and location of the cage inserted, and disc height change, was acquired from the medical records and radiologic images, and the possibility for generating posterior migration of cage was evaluated statistically. Results: The demographic factors and cage-inserted level were similar in the two groups (16 patients in group 1, 32 patients in group 2). In the migration group, number of patients with a pear-type disc, 9 patients, was significantly larger; the disc height change, 1.8 mm, was significantly smaller; and the cage was located frequently on non-center in the anteriorposterior view and center in the lateral view in 9 and 15 out of 16 patients, respectively. Conclusion: A pear-type disc shape, small disc height change, cage with non-center on the anteriorposterior view and non-anterior on the lateral view are the risk factors for posterior migration. These factors are important for preventing posterior migration of the cage.

• Journal of Periodontal and Implant Science
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• v.26 no.4
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• pp.799-821
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• 1996

The ultimate goal of periodontal treatment has been to facilitate regeneration of diseased periodontal tissues, destroyed by inflammatory periodontal disease. For regeneration of the periodontium to occur, all of component tissues must be restored to their original position and architecture. Growth factors which were known to promote the cellular processes, ie, proliferation, migration and matrix synthesis, have been in the spotlight of current periodontics. Platelet-derived growth factor(PDGF) stimulates collagen and non collagen protein synthesis, migration and proliferation of periodontal ligament cells. Insulin-like growth factor(IGF) has potentials to induce collagen and bone matrix synthesis so that it regulates normal bone remodeling. Application of the combination have been known to facilitate formation of bone and cementum, and to synergistically interact to promote coronal migration and proliferation of periodontal ligament cells. These two growth factors have been reported to exhibit positive effect in the periodontally diseased teeth or class m furcation defects. The aim of the present study was to test the hypothesis that PDGF-BB alone or the combination of PDGF-BB and IGF-I can predictably enhance regeneration of the periodontium in the dehiscence defect. Following the resection of premolars, roots were embedded. After 12 weeks of healing period, standardized experimental $4{\times}4mm$ dehiscence defects were created on the mid-facial of the premolar roots in each of 4 young adult dogs. In control group, only methylcellulose gel was inserted in the defects. In experimental group I and II, gel with $2{\mu}g$ of PDGF-BB or $2{\mu}g$ of PDGF-BB and $1{\mu}g$ of IGF-I was inserted in the defects, respectively. At 8 weeks postsurgery, the dogs were sacrificed. The results were observed histologically and analyzed histomorphometrically.The results of this study were as follws. 1. The new cementum formation was $1.26{\pm}0.69mm$ in the control group, $1.80{\pm}0.84mm$ in the experimental group I, $1.93{\pm}0.51mm$ in the experimental group II. The experimental group III, the experimental group I, the control group were in the order of cementum formation without statistically significant differences between control and all experimental groups. 2. The new bone formation was $1.00{\pm}0.53mm$ in the control group, $1.53{\pm}0.63mm$ in the experimental group I, $l.33{\pm}0.45mm$ in the experimental group II. The experimental group I, the experimental group II, the control group were in the order of bone formation without statistically significant differences between control and all experimental groups. 3. The root resorption was $1.12{\pm}0.64mm$ in the control group, $1.34{\pm}0.73mm$ in the experimental group I, $0.79{\pm}0.59mm$ in the experimental group II without statistically significant differences between control and all experimental groups. These results suggested that the use of PDGF-BB alone or PDGF-BB and IGF-I in the dehiscence defects might facilitate periodontal regeneration in some degree, but has not shown statistically significant results.

• Bulletin of the Korean Chemical Society
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• v.26 no.11
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• pp.1823-1825
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• 2005

Angiogenesis is tightly regulated by a variety of angiogenic activators and inhibitors. Disruption of the balanced angiogenesis leads to the progress of diseases such as cancer, rheumatoid arthritis, and diabetic blindness. Even though a number of proteins involved in angiogenesis have been identified so far, more protein factors remain to be identified due to complexity of the process. Here I report that pituitary tumor-transforming gene (PTTG) induces migration and tube formation of human umbilical vein endothelial cells (HUVECs). High levels of both vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are detected in conditioned medium obtained from cells transfected with PTTG expression plasmid. Taken together, these results suggest that PTTG is an angiogenic factor that induces production of both VEGF and bFGF.

• ALGAE
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• v.25 no.3
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• pp.133-140
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• 2010

Using chlorophyll fluorescence, the vertical migration of benthic diatoms responding to light intensity and affected by sediment grain size was studied. Minimal fluorescence ($F_o$) of surface sediment was measured by imaging pulse amplitude modulated (Imaging-PAM) fluorometer, and used to monitor diatom biomass variation in surface sediments. The test diatoms, Amphora coffeaeformis (C. Agardh) K$\ddot{u}$tzing and Cylindrotheca closterium (Ehrenberg) Reimann & Lewin, migrated to the sediment surface under irradiance from 50 to 500 ${\mu}mol$ photons $m^{-2}s^{-1}$. However, the diatoms exhibited no evident increase of surface biomass under dark conditions, and even showed slightly decrease of surface biomass under irradiances over 1,000 ${\mu}mol$ photons $m^{-2}s^{-1}$. The light intensity inducing the maximum surface migration of A. coffeaeformis was 100 ${\mu}mol$ photons $m^{-2}s^{-1}$, while the light intensity producing the same effect for C. closterium was 250 ${\mu}mol$ photons $m^{-2}s^{-1}$. C. closterium showed higher motility than A. coffeaeformis. Faster diatom surfacing was observed in larger grain size sediments (125-335 ${\mu}m$) than smaller ones (63-125 ${\mu}m$). This study confirmed the significant influence of light as a main triggering factor behind migration, indicated the distinct effect of different sediment grain size, and highlighted the species-specific migratory ability.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.3
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• pp.287-292
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• 2017

Vitiligo is an intriguing depigmentary disorder and is notoriously difficult to be treated. The ultimate goal of vitiligo treatment is to replenish the lost melanocytes by immigration from hair follicle and to restore the normal function of melanogenesis by residual melanocytes. There are two types of topical calcineurin inhibitors called tacrolimus and pimecrolimus, and are recommended as the first-line treatments in vitiligo. Although pimecrolimus is efficacious for the repigmentation of vitiligo, its intrinsic mechanisms have never been investigated in vitro. This research aimed to study the ability of pimecrolimus on stimulating melanogenesis, melanocyte migration and MITF (microphthalmia associated transcription factor) protein expression. Results showed that pimecrolimus at the dosages of 1, 10, $10^2$nM were neither mitogenic nor cytotoxic to melanocytes. The addition of pimecrolimus at 10, $10^2$ and $10^3nM$ significantly increased intracellular tyrosinase activity, which was consistent with the elevated content of melanin content at the same concentrations. The peak effect was seen at 72 h in response to $10^2$nM pimecrolimus. Results of the wound scratch assay and Transwell assays indicate that pimecrolimus is effective in facilitating melanocyte migration on a collagen IV-coated surface. In addition, MITF protein yield reached the highest by pimecrolimus at $10^2nM$. In brief, pimecrolimus enhances melanin synthesis as well as promotes migration of melanocytes directly, possibly via their effects on MITF protein expression.

• Journal of Gastric Cancer
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• v.20 no.1
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• pp.95-105
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• 2020

Purpose: Gastric cancer is a highly metastatic malignant tumor, often characterized by chemoresistance and high mortality. In the present study, we aimed to investigate the role of B-cell lymphoma 3 (Bcl-3) protein on cell migration and chemosensitivity of gastric cancer. Materials and Methods: The gastric cancer cell lines, AGS and NCI-N87, were used for the in vitro studies and the in vivo studies were performed using BALB/c nude mice. Western blotting, wound healing assay, Cell Counting Kit-8 assay, immunohistochemistry, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay were used to evaluate the role of Bcl-3 in gastric cancer. Results: We found that the protein expression of hypoxia (HYP)-inducible factor-1α and Bcl-3 were markedly upregulated under hypoxic conditions in both AGS and NCI-N87 cells in a time-dependent manner. Interestingly, small interfering RNA-mediated knockdown of Bcl-3 expression affected the migration and chemosensitivity of the gastric cancer cells. AGS and NCI-N87 cells transfected with si-RNA-Bcl-3 (si-Bcl-3) showed significantly reduced migratory ability and increased chemosensitivity to oxaliplatin, 5-fluorouracil, and irinotecan. In addition, si-Bcl-3 restored the autophagy induced by HYP. Further, the protective role of si-Bcl-3 on the gastric cancer cells could be reversed by the autophagy inducer, rapamycin. Importantly, the in vivo xenograft tumor experiments showed similar results. Conclusions: Our present study reveals that Bcl-3 knockdown inhibits cell migration and chemoresistance of gastric cancer cells through restoring HYP-induced autophagy.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.16 no.7
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• pp.1567-1574
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• 2012

Since a migration method of the mobile agent is a factor that affects the overall performance of the entire distributed system, it is necessary to find efficient migration methods of the mobile agent within the sensor network and to collect and store data related to various components(server, sink and sensor node) of the sensor network, thereby providing consistent naming services. Accordingly, this paper presents design and implementation of MetaTable that is divided into MetaData where information on the sensor data server is stored and SubMetaData where various types of information on sink nodes and data on sensor nodes connected with the sink nodes is stored. Moreover, the paper also presented the implementation of forward migration of an active rule mobile agent applying the naming method based on RMI that used the meta_table and proposed the possibility of constructing efficient sensor network application environment. In this paper, for registration, release and retrieval methods suitable for new sensor network environment, we designed and implemented the naming agent by applying J2EE model based on RMI-IIOP(Internet Inter-ORB Protocol) technique.

• Molecules and Cells
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• v.43 no.8
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• pp.749-762
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• 2020

The migration, dedifferentiation, and proliferation of vascular smooth muscle cells (VSMCs) are responsible for intimal hyperplasia, but the mechanism of this process has not been elucidated. WD repeat domain 1 (WDR1) promotes actin-depolymerizing factor (ADF)/cofilin-mediated depolymerization of actin filaments (F-actin). The role of WDR1 in neointima formation and progression is still unknown. A model of intimal thickening was constructed by ligating the left common carotid artery in Wdr1 deletion mice, and H&E staining showed that Wdr1 deficiency significantly inhibits neointima formation. We also report that STAT3 promotes the proliferation and migration of VSMCs by directly promoting WDR1 transcription. Mechanistically, we clarified that WDR1 promotes the proliferation and migration of VSMCs and neointima formation is regulated by the activation of the JAK2/STAT3/WDR1 axis.