• Journal of Ginseng Research
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• v.43 no.1
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• pp.95-104
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• 2019

Background: Oxidized low-density lipoprotein (ox-LDL) causes vascular endothelial cell inflammatory response and apoptosis and plays an important role in the development and progression of atherosclerosis. Ginsenoside compound K (CK), a metabolite produced by the hydrolysis of ginsenoside Rb1, possesses strong anti-inflammatory effects. However, whether or not CK protects ox-LDL-damaged endothelial cells and the potential mechanisms have not been elucidated. Methods: In our study, cell viability was tested using a 3-(4, 5-dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide (MTT) assay. Expression levels of interleukin-6, monocyte chemoattractant protein-1, tumor necrosis factor-${\alpha}$, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 were determined by enzyme-linked immunosorbent assay and Western blotting. Mitochondrial membrane potential (${\Delta}{\Psi}m$) was detected using JC-1. The cell apoptotic percentage was measured by the Annexin V/ propidium iodide (PI) assay, lactate dehydrogenase, and caspase-3 expression. Apoptosis-related proteins, nuclear factor $(NF)-{\kappa}B$, and mitogen-activated protein kinases (MAPK) signaling pathways protein expression were quantified by Western blotting. Results: Our results demonstrated that CK could ameliorate ox-LDL-induced human umbilical vein endothelial cells (HUVECs) inflammation and apoptosis, $NF-{\kappa}B$ nuclear translocation, and the phosphorylation of p38 and c-Jun N-terminal kinase (JNK). Moreover, anisomycin, an activator of p38 and JNK, significantly abolished the anti-apoptotic effects of CK. Conclusion: These results demonstrate that CK prevents ox-LDL-induced HUVECs inflammation and apoptosis through inhibiting the $NF-{\kappa}B$, p38, and JNK MAPK signaling pathways. Thus, CK is a candidate drug for atherosclerosis treatment.

• Clinical and Experimental Pediatrics
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• v.48 no.6
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• pp.580-587
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• 2005

New evidence is emerging that airway smooth muscle(ASM) may act as an immunomodulatory cell by providing pro-inflammatory cytokines and chemokines, polypeptide growth factors, extracellular matrix proteins, cell adhesion receptors and co-stimulatory molecules. ASM can promote the formation of the interstitial extracellular matrix, and potentially contribute to the alterations within the extracellular matrix in asthma. In addition, extracellular matrix components can alter the proliferative, survival, and cytoskeletal synthetic function of ASM cells through integrin-directed signaling. Increased ASM mass is one of the most important features of the airway wall remodeling process in asthma. Three different mechanisms may contribute to the increased ASM mass : cell proliferation, increased migration and decreased rate of apoptosis. The major signaling pathways of cell proliferation activated by ASM mitogens are those dependent on extracellular signal-regulated kinase and phosphoinositide 3'-kinase. The key signaling mechanisms of cell migration have been identified as the p38 mitogen-activated protein kinase and the p21-activated kinase 1 pathways. ASM cells contain ${\beta}2$-adrenergic receptors and glucocorticoid receptors. They may represent a key target for ${\beta}2$-adrenergic receptor agonist/corticosteroid interactions which have antiproliferative activity against a broad spectrum of mitogens.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.927-932
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• 2016

Bone morphogenetic proteins (BMPs), belonging to the transforming growth factor-${\beta}$ superfamily, regulate many cellular activities including cell migration, differentiation, adhesion, proliferation and apoptosis. Use of recombinant human bone morphogenic protein-2 (rhBMP-2) in oral and maxillofacial surgery has seen a tremendous increase. Due to its role in many cellular pathways, the influence of this protein on carcinogenesis in different organs has been intensively studied over the past decade. BMPs also have been detected to have a role in the development and progression of many tumors, particularly disease-specific bone metastasis. In oral squamous cell carcinoma - the tumor type accounting for more than 90% of head and neck malignancies- aberrations of both BMP expression and associated signaling pathways have a certain relation with the development and progression of the disease by regulating a range of biological functions in the altered cells. In the current review, we discuss the influence of BMPs -especially rhBMP-2- in the development and progression of oral squamous cell carcinoma.

• Polymer(Korea)
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• v.27 no.5
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• pp.397-404
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• 2003

The interaction of cell adhesive protein and polypeptide with bone marrow stromal stem cells (BMSCs) grown in tissue engineered films and scaffolds were examined. Several proteins or polypeptide known as cell-adhesive were coated adsorption on poly(lactide-co-glycolide) (PLGA) films and scaffolds and adhesion and proliferation behavior of BMSC on those surfaces were compared. The protein and polypeptide used include collagen IV, fibrinogen, laminin, gelatin, fibronectin, and poly(L-lysine). The protein and polypeptide were adsorbed on the PLGA film surfaces with almost monolayer coverage except poly(L-lysine). BMSCs were cultured for 1, 2, and 4 days on the protein- or polypeptide-adsorbed PLGA films and scaffolds. The cell adhesion and proliferation behaviors were assessed by sulforho damine B assay. It was observed that the protein- or polypeptide-adsorbed surfaces showed better cell adhesion and proliferation than the control.

• Biomedical Science Letters
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• v.23 no.1
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• pp.44-47
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• 2017

S100A8 and S100A9 are associated with myeloid cell differentiation, chemotactic activities, adhesion of neutrophils, and apoptosis. In this study, we investigated the contribution of S100A8 and S100A9 to differentiation of the human eosinophilic leukemia cell line, EoL-1. S100A8 and S100A9 increased the number of vacuole per one cell and the protein expression of EPO and MBP. Rottlerin, an inhibitor of protein kinase C delta ($PKC{\delta}$), inhibited the EoL-1 cell differentiation induced by S100A8 and S100A9. These results suggest that S100A8 and S100A9 may regulate the differentiation of eosinophilic progenitors. Moreover, these findings may shed light on elucidation of eosinophil differentiation due to S100 proteins.

• Biomaterials and Biomechanics in Bioengineering
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• v.1 no.3
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• pp.163-174
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• 2014

The objective of this study is to prepare an artificial extracellular matrix (ECM) for cell culture by using polymer hydrogels. The polymer used is a cytocompatible water-soluble phospholipid polymer: poly[2-methacryloyloxyethyl phosphorylcholine (MPC)-n-butyl methacrylate-p-nitrophenyloxycarbonyl poly(ethylene oxide) methacrylate (MEONP)] (PMBN). The hydrogels are prepared using a cross-linking reaction between PMBN and diamine compounds, which can easily react to the MEONP moiety under mild conditions. The most favorable diamine is the bis(3-aminopropyl) poly(ethylene oxide) (APEO). The effects of cross-linking density and the chemical structure of cross-linking molecules on the mechanical properties of the hydrogel are evaluated. The storage modulus of the hydrogel is tailored by tuning the PMBN concentration and the MEONP/amino group ratio. The porous structure of the hydrogel networks depends not only on these parameters but also on the reaction temperature. We prepare a hydrogel with $40-50{\mu}m$ diameter pores and more than 90 wt% swelling. The permeation of proteins through the hydrogel increases dramatically with an increase in pore size. To induce cell adhesion, the cell-attaching oligopeptide, RGDS, is immobilized onto the hydrogel using MEONP residue. Bovine pulmonary artery endothelial cells (BPAECs) are cultured on the hydrogel matrix and are able to migrate into the artificial matrix. Hence, the RGDS-modified PMBN hydrogel matrix with cross-linked APEO functions as an artificial ECM for growing cells for applications in tissue engineering.

• Applied Chemistry for Engineering
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• v.32 no.4
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• pp.371-378
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• 2021

The formation of hydrophilic surface based on polymers has received great attention due to the anti-adhesion of bacteria on solid substrates. Anti-adhesion coatings are aimed at suppressing the initial step of biofilm formation via non-cytotoxic mechanisms, and surfaces applied hydrophilic or ionic polymers showed the anti-adhesion effect for bioentities, such as proteins and bacteria. This is attributed to the formation of surface barrier from hydration layers, repulsions and osmotic stresses from polymer brushes, and electrostatic interactions between ionic polymers and cell surfaces. The antifouling polymer coating is usually fabricated by the grafting method through the bonding with functional groups on surfaces and the deposition method utilizing biomimetic anchors. This mini-review is a summary of representative antifouling polymers, coating strategies, and antibacterial efficacy. Furthermore, we will discuss consideration on the large area surface coating for application to public facilities and industry.

• Journal of Animal Reproduction and Biotechnology
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• v.35 no.1
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• pp.12-20
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• 2020

Cell adhesion plays an important role in the differentiation of the morphogenesis and the trophectoderm epithelium of the blastocyst. In the porcine embryo, CDH1 mediated adhesion initiates at compaction before blastocyst formation, regulated post-translationally via protein kinase C and other signaling molecules. Here we focus on muscle RAS oncogene homolog (M-RAS), which is the closest relative to the RAS related proteins and shares most regulatory and effector interactions. To characterize the effects of M-RAS on embryo compaction, we used gain- and loss-of-function strategies in porcine embryos, in which M-RAS gene structure and protein sequence are conserved. We showed that knockdown of M-RAS in zygotes reduced embryo development abilities and CDH1 expression. Moreover, the phosphorylation of ERK was also decreased in M-RAS KD embryos. Overexpression of M-RAS allows M-RAS KD embryos to rescue the embryo compaction and blastocyst formation. Collectively, these results highlight novel conserved and multiple effects of M-RAS during porcine embryo development.

• Molecules and Cells
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• v.39 no.7
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• pp.557-565
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• 2016

The paired immunoglobulin-like type 2 receptor (PILR) family consists of two functionally opposite members, inhibitory $PILR{\alpha}$ and activating $PILR{\beta}$ receptors. PILRs are widely expressed in various immune cells and interact with their ligands, especially CD99 expressed on activated T cells, to participate in immune responses. Here we investigated whether PILR-derived agonists inhibit ${\beta}1$ integrin activity as ligands for CD99. PILR-derived peptides as well as PILR-Fc fusion proteins prevented cell adhesion to fibronectin through the regulation of ${\beta}1$ integrin activity. Especially, PILRpep3, a representative 3-mer peptide covering the conserved motifs of the PILR extracellular domain, prevented the clustering and activation of ${\beta}1$ integrin by dephosphorylating FAK and vinculin, which are major components of focal adhesion. In addition, PILRpep3 inhibited transendothelial migration of monocytes as well as endothelial cell tube formation. Furthermore, upon intraperitoneal injection of PILRpep3 into mice with collagen-induced arthritis, the inflammatory response of rheumatoid arthritis was strongly suppressed. Taken together, these results suggest that PILR-derived agonist ligands may prevent the inflammatory reactions of rheumatoid arthritis by activating CD99.

• Korean Journal of Veterinary Service
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• v.42 no.2
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• pp.73-83
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• 2019

Foot-and-Mouth Disease (FMD) is a highly contagious trans-boundary viral disease caused by FMD virus, which causes huge economic losses. FMDV infects cloven hoofed (two-toed) mammals such as cattle, sheep, goats, pigs and various wildlife species. To control the FMDV, it is necessary to understand the life cycle and the pathogenesis of FMDV in host. Especially, the protein-protein interaction between FMDV and host will help to understand the survival cycle of viruses in host cell and establish new therapeutic strategies. However, the computational approach for protein-protein interaction between FMDV and pig hosts have not been applied to studies of the onset mechanism of FMDV. In the present work, we have performed the prediction of the pig's proteins which interact with FMDV based on RNA-Seq data, protein sequence, and structure information. After identifying the virus-host interaction, we looked for meaningful pathways and anticipated changes in the host caused by infection with FMDV. A total of 78 proteins of pig were predicted as interacting with FMDV. The 156 interactions include 94 interactions predicted by sequence-based method and the 62 interactions predicted by structure-based method using domain information. The protein interaction network contained integrin as well as STYK1, VTCN1, IDO1, CDH3, SLA-DQB1, FER, and FGFR2 which were related to the up-regulation of inflammation and the down-regulation of cell adhesion and host defense systems such as macrophage and leukocytes. These results provide clues to the knowledge and mechanism of how FMDV affects the host cell.