• Journal of Microbiology and Biotechnology
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• v.13 no.2
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• pp.276-281
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• 2003

The adhesion of probiotic bacteria to the intestinal mucosa is one of the desirable properties for their colonization in the intestinal tract, where these bacteria constantly compete with other bacteria. The adhesion of different strains of bifidobacteria to Caco-2 cells was compared. Among the strains examined, BGN-4 showed the highest adhesion level and the greatest cell surface hydrophobicity (CSH). No close relationship was found between the adhesion and CSH of the strains. Upon protease and heat treatment, the adhesion of the BGN-4 to the Caco-2 cells decreased significantly. The cells grown at $42^{\circ}C$ showed a lower CSH and self-aggregation levels than cells grown at $37^{\circ}C$. The treatment of EGTA did not have any effect on the adhesion. The degree of adhesion did not differ among the experimental groups in which galactose, mannose, or fucose were added in the adhesion assay mixture. The results suggest that the adhesion of the Bifidobacterium to the epithelial cells may be affected by the composition and structure of the cell membrane and interacting surfaces.

• Journal of Animal Reproduction and Biotechnology
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• v.38 no.3
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• pp.121-130
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• 2023

Background: Coating a culture plate with molecules that aid in cell adhesion is a technique widely used to produce animal cell cultures. Extracellular matrix (ECM) is known for its efficiency in promoting adhesion, survival, and proliferation of adherent cells. Gelatin, a cost-effective type of ECM, is widely used in animal cell cultures including feeder-free embryonic stem (ES) cells. However, the optimal concentration of gelatin is a point of debate among researchers, with no studies having established the optimal gelatin concentration. Methods: In this study, we coated plastic plates with gelatin in a concentration-dependent manner and assessed Young's modulus using atomic force microscopy (AFM) to investigate the microstructure of the surface of each plastic plate. The adhesion, proliferation, and differentiation of the ESCs were compared and analyzed revealing differences in surface microstructure dependent on coating concentration. Results: According to AFM analysis, there was a clear difference in the microstructure of the surface according to the presence or absence of the gelatin coating, and it was confirmed that there was no difference at a concentration of 0.5% or more. ES cell also confirmed the difference in cell adhesion, proliferation, and differentiation according to the presence or absence of gelatin coating, and also it showed no difference over the concentration of 0.5%. Conclusions: The optimum gelatin-coating for the maintenance and differentiation of ES cells is 0.5%, and the gelatin concentration-mediated microenvironment and ES cell signaling are closely correlated.

• Bulletin of the Korean Chemical Society
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• v.34 no.8
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• pp.2525-2527
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• 2013

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1152-1156
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• 2007

The Camella japonica flower(CJF) extract was studied for their anti-angiogenenic and anti-cell adhesion effect. CJF-extract inhibited the tube formation on human umbilical vein endotherial cells(HUVEC) with butanol extract by 70.2%, acetone extract by 54.2%, ethyl acetate extract by 37.0%, chloroform extract by 21.2%. Cell adhesion molecules were effectively suppressed at different concentration of CJF at 50, 100, 200 ug/well such as for intercellular adhesion molecule(ICAM) by 5.9%, 29.4% and 52.9%, for vascular cell adhesion molecule(VCAM) by 12.5%, 43.8% and 62.5%, for E-selectin by 7.1%, 21.4% and 35.7%, respectively. Signal molecules of vascular endotherial growth factor receptor 2(VEGFR2), ${/beta}$-catenin and PI3K are inhibited by different concentration of CJF at 10, 20 and 30 ${\mu}g/mL$ with western blot. Angiogenesis will be inhibited with suppressing NF-kB molecule resulted in signal molecules blocked by CJF. CJF will be useful materials for treatment of angiogenesis related diseases such as cancer, metastasis, rheumathioid arthritis and obesity.

• Animal cells and systems
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• v.5 no.3
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• pp.253-262
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• 2001

Ligand-receptor clustering event is the most important step in leukocyte adhesion and spreading on endothelial cells. Intercellular adhesion molecule-1 (ICAM-1) has been shown to enhance leukocyte adhesion, but the molecular event during the process of adhesion is unclear. To visualize the dynamics of ICAM-1 movement during adhesion, we have engineered stable Chinese hamster ovary cell lines expressing ICAM-1 fused to a green fluorescent protein (IC1_GFP/CHO) and examined them under the fluorescence microscopy. The transfection of IC1_GFP alone in these cells was sufficient to support the adhesion of K562 cells that express $\alpha$L$\beta$2 (LFA-1) integrin stimulated by CBR LFA-1/2 mAb. This phenomenon was mediated by ICAM-1-LFA-1 interactions, as an mAb that specifically inhibits ICAM-1-LFA-1 interaction (RRl/l) completely abolished the adhesion of LFA-1＊ cells to IC1_ GFP/CHO cells. We found that the characteristic of adhesion was followed almost immediately (~10 min) by the rapid accumulation of ICAM-1 on CHO cells at a tight interface between the two cells. Interestingly, ICI_GFP/CHO cells projected plasma membrane and encircled approximately half surface of LFA-1+ cells, as defined by confocal microscopy. This unusual phenomenon was also confirmed on HUVEC after adhesion of LFA-1＊ cells. Neither cytochalasin D nor 2,3-butanedione 2-monoxime an inhibitor of myosin light chain kinase blocked LFA-1-mediated ICAM-1 clustering, indicating that actin cytoskeleton and myosin-dependent contractility are not necessary for ICAM-1 clustering. Taken together, we suggest that leukocyte adhesion to endothelial cells induces specialized form of ICAM-1 clustering that is distinct from immunological synapse mediated by T cell interaction with antigen presenting cells.

• YAKHAK HOEJI
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• v.51 no.6
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• pp.482-489
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• 2007

Kaempferitrin, isolated from Kenaf (Hibiscus cannabinus), was examined to evaluate its modulatory effects on antigen-presenting cell functions of macrophages/monocytes such as phagocytosis of foreign materials, up-regulation of costimulatory molecules (CD40, CD80 and CD86), adhesion molecule activation, and antigen processing and presentation. Kaempferitrin strongly blocked up-regulation of CD40, CD80 and CD86, but not pattern recognition receptor (PRR) (e.g., TLR2). It also suppressed functional activation of CD29 (${\beta}1$-integrins), as assessed by cell-cell adhesion assay, required for T cell-antigen-presenting cell (APC) interaction. Furthermore, this compound did not block a simple activation of CD29, as assessed by cell-fibronectin adhesion assay. However, the compound did not diminish phagocytic uptake, an initial step for antigen processing, and ROS generation in RAW264.7 cells. In particular, to understand molecular mechanism of kaempferitrin-mediated inhibition, the regulatory role of LPS-induced signaling events was examined using immunoblotting analysis. Interestingly, this compound dose dependently suppressed the phosphorylation of $I{\kappa}B{\alpha}$, Src, Akt and Syk, demonstrating that it can negatively modulate the activation of these signaling enzymes. Therefore, our data suggested that kaempferitrin may be involved in regulating APC function-relevant immune responses of macrophages and monocytes by regulating intracellular signaling.

• The Journal of Korean Society of Virology
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• v.26 no.1
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• pp.47-58
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• 1996

Histopathological vascular changes in hemorrhagic fever with renal syndrome (HFRS) caused by Hantaan virus include increased vascular permeability, disseminated intravascular coagulation, thrombocytopenia and changes in coagulation activity. Although vascular endothelial cells of main target organs such as kidney infected with Hantaan virus are not damaged but swelling of endothelial cells, perivascular exudates and infiltration of mononuclear cells and fresh interstitial hemorrhages are common. However, the pathogenesis of cell infiltration and hemorrhages around vascular endothelial cells are not well understood. Some endothelial cell molecules or vascular adhesins that acts as adhesion moleulces for leukocyte are expressed on endothelial cells close to site of inflammation. However, whether the expression of endothelial adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule (ICAM-1) and endothelial leukocyte adhesion molecule (ELAM) on vascular endothelial cells are increased by infection with Hantaan virus has not been studied. In this study, the relationship between the expression of VCAM-1, ICAM-1 and ELAM and adhesion of mononuclear cells on endothelial cells of human blood vessels infected with Hantaan virus was investigated. The endothelial cells of umbilical vein was passaged three times in culture medium and the monolayered cells were infected with $10^5\;pfu/ml$ of Hantaan virus grown in Vera E6 cell cultures. The multiplication of virus in cultured endothelial cells was monitored by immunohistochemistry and the expression of adhesion molecules was demonstrated by immunohistochemistry using monoclonal antibodies against VCAM-1, ICAM-1 and ELAM. And in situ hybriditation against ICAM-1 was also performed. The endothelial adhesion molecules, VCAM and ICAM, were expressed after 6 hours postinfection, respectively, and their expressions lasted for 72 hours. Similar expression of VCAM and ICAM appeared on endothelial cells by infection with virus, but the expression of ELAM was not recognized up to 72 hours postinfection. Microscopically, it was noted that many monocuclear cells adhered on endothelial cells infected with viruses. In an electronmicroscopic study, the transendothelial migration of mononuclear cells was observed on monolayered endothelial cells infected with virus. This results suggested that the endothelial adhesion molecules, particulary VCAM and ICAM, might be expressed on endothelial cells by infection with Hantaan virus and these molecules play a key role in the adhesion and extravasation of inflammatory cells around blood vessels.

• Proceedings of the KSME Conference
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• 2005.11a
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• pp.69.1-69.1
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• 2005

• Proceedings of the Korean Vacuum Society Conference
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• 2013.08a
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• pp.275-275
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• 2013

Osteoblast is one of cells related with osseointegration and many research have conducted the adhesion of osteoblast onto the surface of implant. In the osseointegration, biocompatibility of the implant and cell adhesion to the surface are important factors. The researches related to cell adhesion have a direction from micro-scaled surface roughness to nano-scaled surface roughness with advancing nanotechnology. A cell reacts and sense to stimuli from extracellular matrix (ECM) and topography of the ECM [1]. Thus, for better osseointegration, we should provide an environment similar to ECM. In this study, we synthesize TiO2 nanowires using hydrothermal reaction because TiO2 provides inertness to titanium on its surface and enables it used as an implant material for the orthopedic treatment such as fixation of the bone fracture [2]. Ti substrate is immersed into NaOH aqueous solution. The solution are heated at $140{\sim}200^{\circ}C$ for various time (10~720 minutes). After heat treatment, we take out the sample and immerse it into HCl aqueous solution for 1 hour. The acid treated sample is heated again at $500^{\circ}C$ for 3 hours [3]. Then, we culture osteoblast on the TiO2 nanowires. For investigating cell adhesion onto nanostructured surface, we conduct several tests such as MTT assay, ALP (Alkaline phosphatase) activity assay, measuring calcium expression, and so on. These preliminary results of the cell culture on the nanowires are foundation for investigating cell-material interaction especially with nanostructure interaction.

• Journal of the Korean Society of Food Science and Nutrition
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• v.31 no.6
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• pp.1134-1141
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• 2002

Adhesion of leukocytes to the activated vascular endothelium and their subsequent recruitment/migration into the artery wall are key features in the pathogenesis of atherosclerosis and inflammatory diseases. These features have been mediated by cell adhesion molecules including vascular cell adhesion molecule-1 (VCAM-1) and in tracellular cell adhesion molecule-1 (ICAM-1). This study examined whether flavonoids inhibit the pro-inflammatory cytokine TNF-$\alpha$-induced monocyte adhesion via a modulation of the protein expression of VCAM-1 and ICAM-1 of human umbilical vein endothelial cells (HUVECs). TNF-$\alpha$ markedly increased the adhesion of THP-1 monocytes to endothelial cells and induced the expression of VCAM-1, ICAM-1 and E-selectin proteins in HUVECs. Micromolar concentrations of the flavones luteolin and apigenin and the flavonol quercetin near completely blocked the monocyte adhesion to the activated endothelial cells and the induction of these adhesion molecules. However, equimicromolar catechins of (-)epigallocatechin gallate and (+)catechin, the flavonol myr- icetin and the flavanones of naringin and hesperidin had no effect on TNF-$\alpha$-activated monocyte adhesion. (-)Epigallocatechin gallate, (+) catechin, and naringin did not attenuate the TNF-$\alpha$ induction of these adhesion molecules. Furthermore, culture with luteolin and apigenin strongly blocked the expression of TNF-$\alpha$-induced VCAM-1 mRNA and modestly attenuated ICAM-1 mRNA. Quercetin modestly decreased the TNF-$\alpha$-activated VCAM-1 and ICAM-1 mRNAs. These results demonstrate that flavonoids classified as flavones and flavonols may inhibit monocyte adhesion to the TNF-$\alpha$-activated endothelium, most likely due to a blockade of expression of functional adhesion molecules down-regulated at the transcriptional level, indicating a definite linkage between the chemical structure of flavonoids and the expression of cell adhesion molecules. Furthermore, the antiathero-genic feature of flavonoids appears to be independent of their antioxidant activity.