• Journal of Gastric Cancer
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• v.12 no.3
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• pp.140-148
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• 2012

Purpose: Among cell adhesion molecules, serum levels of intercellular adhesion molecule-1 and E-selectin are known to be correlated with the metastatic potential of gastric cancer. In the present study, the authors investigated the expression of intercellular adhesion molecule-1 and E-selectin in gastric cancer tissues and cultured gastric cancer cells, and examined their clinical value in gastric cancer. Materials and Methods: The protein was extracted from gastric cancer tissues and cultured gastric cancer cells (MKN-28 and Kato-III) and the expression of intercellular adhesion molecule-1 and E-selectin was examined by western blotting. The clinical significance of intercellular adhesion molecule-1 and E-selectin was explored, using immunohistochemical staining of specimens from 157 gastric cancer patients. Results: In western blot analysis, the expressions of intercellular adhesion molecule-1 in gastric cancer tissues and cultured gastric cancer cells were increased, however, E-selectin in gastric cancer tissues and cells were not increased. Among 157 gastric cancer patients, 79 patients (50%) were intercellular adhesion molecule-1 positive and had larger tumor size, an increased depth of tumor invasion, lymph node metastasis and perineural invasion. The intercellular adhesion molecule-1 positive group showed a higher incidence of tumor recurrence (40.5%), and a poorer 3-year survival than the negative group (54.9 vs. 85.9%, respectively). Conclusions: Intercellular adhesion molecule-1 is overexpressed in gastric cancer tissues and cultured gastric cancer cells, whereas E-selectin is not overexpressed. Increased expression of intercellular adhesion molecule-1 in gastric cancer could be related to the aggressive nature of the tumor, and has a poor prognostic effect on gastric cancer.

• The Korea Journal of Herbology
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• v.22 no.4
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• pp.137-143
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• 2007

Objectives : Catalpa ovata G. Don (Bignoniaceae) has been shown to possess a variety of pharmacological activities. However, the effect of Catalpa ovata G. Don on endothelial adhesion molecule expression has not been reported. Methods : To examine the effect of Catalpa ovata G. Don on the expression of adhesion molecules in human umbilical vein endothelial cells (HUVECs) stimulated with tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), we used various methods such as Western blot analysis, reverse tranascription-polymerase chain reaction (RT-PCR), and luciferase activity assay. Results : 1. The extract of Catalpa ovata G. Don inhibited the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in HUVECs stimulated with TNF-${\alpha}$. 2. The extract of Catalpa ovata G. Don reduced TNF-${\alpha}$-induced adhesion of leukocytes to HUVECs. 3. In addition, The extract of Catalpa ovata G. Don inhibited the promoter activities of ICAM-1 and VCAM-1. Conclusions : These results that Catalpa ovata G. Don may be beneficial in the treatment of inflammatory such as atherosclerosis.

• Journal of Periodontal and Implant Science
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• v.26 no.3
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• pp.655-668
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• 1996

The change in vascular adhesion molecule expression and number of infiltrating leukocytes were investigated irnmunohistochemically in clinically healthy and inflammed gingiva. Monoclonal antibodies to ICAM-1, VCAM-1 and E-cadherin were used to identify positive vessels and leukocyte within gingival biopsies. 10 healthy gingiva and 30 inflammed gingiva was resected by clinical crown lengthening and modified Widman flap operation, respectively. Leukocyte entry into tissues at sites of inflammation is controlled by the interaction between adhesion molecule and endothelium. Because of rapid and severe destructive periodontal disease that is remarkable leukocyte adhesion deficiency, it is very important to unerdstand the mechanism of host defence against periodontal disease. The purpose of this investigation was the characterization of the presence and distribution of the adhesion molecule(ICAM-1, VCAM-1 and Evcadherin) in inflammatory gingival tissues compared to clinically healthy gingiva. The results were as followed; 1. ICAM-1 was distributed on basal layer, endothelium and mononuclear cells 10 healthy gingiva but inflammed gingiva was observed stronger stain than healthy gingiva. 2. Rare expression was observed in both group but few positive VCAM-1 cells were investigated in inflammatory gingival tissues 3. E-cadherin was expressed in only epithelium and reduced expression was observed in inflammatory gingival tissues. ICAM-1, VCAM-1 showed more expression in inflammatory tissues compared to healthy gingiva. Conversely, E-cadherin revealed a opposite result. These finding demonstrate a characteristic distribution and degree of adhesion molecule in healthy and inflammatory gingival tissues. But it is suggested that more detail study be progressive associated with leukocyte adhesion molecule to determine characterization of periodontal disease.

• Korean Journal of Bronchoesophagology
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• v.5 no.2
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• pp.174-181
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• 1999

The palatine tonsils(tonsils) and pharyngeal tonsils(adenoids) are situated at the entrance of the respiratory and alimentary tracts and represent the first site of contact with a variety of microorganisms and other antigens present in food and inhaled air. They are known as lymphoid organs carrying out the function of cellular and humoral immunity, and so they form a local protective barrier. And the expression of the vascular endothelial adhesion molecules is known to play an important role for the inflammatory reaction in tonsils and adenoids as well as in other inflammatory tissues, by binding with the receptors on the surface of leukocytes. But although several scientific hypotheses on the role of these lympoid tissues have been suggested, their complete functions have remained unknown. The purpose of this study is to present an basic data of the knowledge on the immunologic physiology of the tonsils and adenoids and their role as active immunologic organs that reinforce the mucosal immunity of the entire upper aerodigestive tract. We examined 16 human tonsils and adenoids and the expression of three endothelial adhesion molecules, vascular endothelial adhesion molecule-1(VCAM-1), intracellular adhesion molecule-1(ICAM-1), and E-selection, in tissue sections using immunohistochemistry. We used the inferior turbinate mucosa obtained from 9 patients getting septal surgery as a control group. The expressions of vascular endothelial adhesion molecule-1(VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) were significantly higher in the tonsils and adenoids. But respectively, there were no significant differences between the tonsils and adenoids. The expression of E-selection was significant higher in the tonsils, but not in the adenoids. We observed that tonsils and adenoids showed significantly higher expressions of vascular endothelial adhesion molecule-1(VCAM-1), intracellular adhesion molecule-1(ICAM-1), and E-selection (in the case of E-selection, only in the tonsils). We propose that these adhesion molecules play an important role for the immunologic reaction by the transendothelial migration of lymphocytes and binding with the receptors on the surface of leukocytes.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.221.2-222
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• 2003

Expressions of cellular adhesion molecules (CAMs) are closely related to the formation of early atherosclerosis, an age-dependent vascular disorder. However. previous research provided only limited and conflicted reports on age-related alterations of CAMs' expressions and even much less is known the modulation of CAMs by calorie restriction (CR), In this study, expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, P-selectin and platelet/endothelial cell adhesion molecule-1 (PECAM-1) in aorta and kidney were investigated by western blot and immuno-histochemical stain utilizing ad libitum (AL) and CR rat. (omitted)

• Journal of Nutrition and Health
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• v.31 no.8
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• pp.1235-1243
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• 1998

Although an elevated plasma level of high density lipoprotein (HDL) is known as a protective component against the development of atherosclerosis and ensuing coronary heart diseases, the related mechanisms are still not established . It has been clearly demonstrated in the early stages of atherogenesis that adhesion of monocytes and lymphocytes to the vascular endothelium is enhanced via adhesion molecules, and that monocytes and macrophages accumulate in the subendothelial space. The present study has investigated whether isolated plasma HDL plays a role in protection against atherogenesis by inhibiting the expression of vascular cell adhesioin molecule-1(VCAM-1) on the endothelial cells. Effects of plasma native low density lipoprotein (LDL) and ac ethylated LDL(AcLDL) on VCAM-1 expression were also examined by using an immunocytochemical technique. While plasma HDL did not alter the basal expression of VCAM-1 , lipopolysaccharide(LPS) induction of this adhesion modlecule was markedly inhibited at a phyaiological concentration of HDL. In contrast, 30$\mu\textrm{g}$ protein/ml AcLDL increased sifnificantly both basal VCAM-1 expression and its LPD induction , suggesting that this modified LDL enhances leukocyte adhesiion to endothelial cells. Unlike AcLDL , plasma native LDL inhibited significantly VCAM-1 expression. This indicates that LDL did not undergo oxidative modificantion while incubated with endothelial cells. These results suggest that plasam HDL may inhibit atherogenesis by reducing the expression of adhesion molecules, which is a protective mechanism independent of tis reverse cholesterol transport function . Modified LDL is a potent iducer for adhesion molecules in vascular endothelical cells and could play a role in the pathogenesis of atherosclerosis by adhering to blood cells.

• Biomolecules & Therapeutics
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• v.12 no.3
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• pp.145-150
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• 2004

Inflammation is a frequent radiation-induced reaction following therapeutic irradiation. Treatment of human umbilical endothelial cells (HUVEC) with ${\gamma}$-irradiation (${\gamma}$IR) induces the expression of adhesion proteins such as intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Since the upregulation of these proteins on endothelial cell Surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. In the present study, we demonstrate that vitamin C inhibits ${\gamma}$IR induced expression of ICAM-1, VCAM-1, and E-selectin on HUVEC in a dose- and time dependent manner. Vitamin C a1so inhibited the production of Nitric oxide (NO) induced by ${\gamma}$IR. These data suggest that vitamin C has therapeutic potential for the treatment of various inflammatory disorder associated with an increase of endothelial leukocyte adhesion molecules.

• Journal of Microbiology and Biotechnology
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• v.11 no.6
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• pp.922-927
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• 2001

In an effort to regulate the mammalian cell behavior in entrapment with a gel, we have functionalized hydrogels with the putative cell-binding (-Arg-Gly-Asp-)(RGD) domain. An adhesion molecule of Gly-Arg-Gly-Asp-Ser (GRGDS) peptides, a cell recognition ligand, was induced into thermo-reversible hydrogels, composed of N-isopropylacrylamide with small amounts of acrylic acid (typically 2-5 $mol\%$ in feed), as a biomimetic extracellular matrix (ECM). The GRGDS containing a p(NiPAAm-co-AAc) copolymer gel was studied in vitro for its ability to promote the spreading and viability of cells by introducing a GRGDS sequence. Hydrogel with no adhesion molecule was a poor ECM for adhesion, permiting spreading of only $3\%$ of the seeded cells for 36h. By immobilizing the peptide linkage into the hydrogel, the conjugation of RGD promoted $50\%$ of proliferation for 36h. However, the GREDS sequence, nonadhesive peptide linkage, conjugated hydrogel showed only $5\%$ of the seeded cell for the same time period. In addition, with the serum-free medium, only GRGDS peptides conjugated to hydrogel was able to promotecell spreading, while there was no cell proliferation in the hydrogel without GRGDS. Thus, the GRGDS peptide-conjugated thermo-reversible hydrogel specifically mediated the cell spreading. This result suggests that utilization of peptide sequences conjugating with the cell-adhesive motifs can enhance the degree of cell surface interaction and influence the long-term formation of ECM in vitro.

• 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.

• Journal of Ginseng Research
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• v.32 no.3
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• pp.244-249
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• 2008

Vascular inflammation is an important step in the development of cardiovascular disorder. Since it has not been known whether Korean red ginseng has a role to play on the vascular inflammation, we investigated the effects of Korean red ginseng extract (KRGE) on monocyte adhesion and its underlying signaling mechanism. Monocyte adhesion assay and Western blot were conducted on the human umbilical vein endothelial cells to study monocyte adhesion and the expression of adhesion molecules. Intracellular calcium was measured with Fura-2 fluorescent staining, and superoxide production was measured with lucigenin chemiluminescence in the endothelial cells. KRGE inhibits tumor necrosis factor (TNF)-alpha-induced monocyte adhesion on the endothelial cells at the range of $0.03{\sim}1$ mg/ml. TNF-alpha-induced vascular cell adhesion molecule-1 and intercellular cell adhesion molecule-1 expression were inhibited by the pretreatment of KRGE in the endothelial cells. KRGE also inhibits TNF-alpha-induced intracellular calcium and the superoxide production in the endothelial cells. This study first demonstrated that KRGE inhibits TNF-alpha-induced monocyte adhesion by inhibiting the adhesion molecule expression, intracellular calcium and superoxide production in the endothelial cells. Therefore, the anti-inflammatory function of KRGE may be contributed to protecting the endothelial dysfunction in the vascular inflammatory disorders.