• Proceedings of the PSK Conference
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• 2003.10b
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• pp.130.3-131
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• 2003

Inflammation is a frequent radiation-induced following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. We examined the effect if allicin, a major component of garlic, on the induction of intercellular adhesion molecule-l (ICAM-1) by gamma-irradiation and the mechanisms of its effect in gamma-irradiated human umbilical vein endothelial cells (HUVECs). (omitted)

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.3
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• pp.191-198
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• 2017

Background: For peripheral nerve regeneration, recent attentions have been paid to the nerve conduits made by tissue-engineering technique. Three major elements of tissue-engineering are cells, molecules, and scaffolds. Method: In this study, the attachments of nerve cells, including Schwann cells, on the nerve conduit and the effects of both growth factor and adhesion molecule on these attachments were investigated. Results: The attachment of rapidly-proliferating cells, C6 cells and HS683 cells, on nerve conduit was better than that of slowly-proliferating cells, PC12 cells and Schwann cells, however, the treatment of nerve growth factor improved the attachment of slowly-proliferating cells. In addition, the attachment of Schwann cells on nerve conduit coated with fibronectin was as good as that of Schwann cells treated with glial cell line-derived neurotrophic factor (GDNF). Conclusion: Growth factor changes nerve cell morphology and affects cell cycle time. And nerve growth factor or fibronectin treatment is indispensable for Schwann cell to be used for implantation in artificial nerve conduits.

• Nutrition Research and Practice
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• v.7 no.1
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• pp.9-14
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• 2013

Bamboo leaves (Phyllostachys pubescens Mazel ex J. Houz (Poacea)) have a long history of food and medical applications in Asia, including Japan and Korea. They have been used as a traditional medicine for centuries. We investigated the mechanism of anti-inflammatory activity of a bamboo leaf extract (BLE) on tumor necrosis factor-alpha (TNF-${\alpha}$)-induced monocyte adhesion in human umbilical vein endothelial cells (HUVECs). Exposure of HUVECs to BLE did not inhibit cell viability or cause morphological changes at concentrations ranging from 1 ${\mu}g/ml$ to 1 mg/ml. Treatment with 0.1 mg/ml BLE caused 63% inhibition of monocyte adhesion in TNF-${\alpha}$-activated HUVECs, which was associated with 38.4% suppression of vascular cell adhesion molecule-1 expression. Furthermore, TNF-${\alpha}$-induced reactive oxygen species generation was decreased to 47.9% in BLE treated TNF-${\alpha}$-activated HUVECs. BLE (0.05 mg/ml) also caused about 50% inhibition of interleukin-6 secretion from lipopolysaccharide-stimulated monocyte. The results indicate that BLE may be clinically useful as an anti-inflammatory or anti-oxidant for human cardiovascular disease including atherosclerosis.

• Korean Journal of Pharmacognosy
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• v.33 no.4 s.131
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• pp.343-351
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• 2002

Atherosclerosis is a progressive disease characterized by the accumulation of lipids and fibrous elements in the arteries. Monocyter/macrophages are involved in many aspects of the development of atherosclerotic plaques. It is known that the intercellular adhesion molecule-1(ICAM-1) expressed preferentially on endothelial cells of atherosclerotic plaque, promotes local adhesion and transendothelial migration of monocytes, neutrophils, and lymphocytes. Using the human promyelocytic leukemia HL-60 cell line, we investigated the inhibitory effects of methanol extracts of 175 natural plants on ICAM-1/LFA-1 mediated cell adhesion. Eight kinds of methanol extracts of tested plants inhibited PMA-induces homotypic aggregationof HL-60 cells without cytotoxicity at the concentration of $6.25\;{\mu}g/ml$. They were divided two fractions of $CHCI_3$ and $H_2O$ to use solvent partition. Among them, $CHCI_3$ extract $(1.0\;{\mu}g/ml)$ of Saururus chinensis and Chloranthus japonicus singificantly inhibited aggregation of HL-60 cells without cytotoxicity, respectively.

• Animal cells and systems
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• v.14 no.4
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• pp.275-282
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• 2010

Chunghyul-dan (CHD) is a combinatorial drug known to exert anti-inflammatory effects in endothelial cells. In this study, we employed global transcriptional profiling using cDNA microarrays to identify molecular mechanisms responsible for the anti-inflammatory activity of CHD in endothelial cells. An analysis of the microarray data revealed that transcript levels of monocyte chemotactic protein-1 (MCP-1), vascular cell-adhesion molecule-1 (VCAM-1) and activated leukocyte cell-adhesion molecule were dramatically altered in CHD-treated endothelial cells. These changes in gene expression were confirmed by RT-PCR, Western blotting and ELISA. Chronic CHD treatment also appeared to decrease MCP-1 secretion, probably as a result of decreased MCP-1 expression. In addition, we determined that chronic CHD treatment inhibited lipopolysaccharide-stimulated adhesion of THP-1 leukocytes to endothelial cells. The inhibitory effect of CHD on LPS-stimulated adhesion resulted from downregulation of VCAM-1 expression. Transmigration of THP-1 leukocytes through endothelial cells was also inhibited by chronic CHD treatment. In conclusion, CHD controls a variety of inflammatory activities by regulating MCP-1 and VCAM-1 gene expression.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.5
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• pp.635-641
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• 2011

Anti-atherogenic effects in tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated human umbilical vein endothelial cells (HUVEC) are involved with suppressed oxidative stress, cell adhesion molecules, and pro-inflammatory factors. The aim of this study was to determine whether green tea seed coat ethyl acetate fraction (GTSCE) could modulate cell adhesion molecules and inflammatory mediators in HUVEC stimulated with TNF-${\alpha}$. Nitric oxide (NO) production was significantly increased in TNF-${\alpha}$-stimulated HUVEC compared to TNF-${\alpha}$ only treated cells. The NO that is produced by endothelial nitric oxide synthase dilates blood vessels and has protective effects against platelet and leucocyte adhesion. GTSCE at 25, 50, 75, and $100\;{\mu}g$/mL significantly (p<0.05) reduced TNF-${\alpha}$ production. GTSCE significantly (p<0.05) inhibited soluble vascular cell adhesion molecule-1 level, in a dose-dependent manner. Monocyte chemoattractant protein-1 level was also significantly (p<0.05) inhibited by GTSCE treatment at $75\;{\mu}g$/mL compared to the TNF-${\alpha}$-only treated group. Total antioxidant capacity by GTSCE was significantly (p<0.05) enhanced compared to the TNF-${\alpha}$-only treated group. These results suggest that GTSCE can inhibit the production of cell adhesion molecules and inflammatory mediators and could be used as a candidate bioactive material to prevent the development of atherosclerosis.

• Molecules and Cells
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• v.28 no.3
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• pp.183-188
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• 2009

TSAd/Lad is a T cell adaptor molecule involved in $p56^{lck}$-mediated T cell activation. To investigate the functions of TSAd in T cells, we generated transgenic (TG) mice expressing the SH2 domain of TSAd (TSAd-SH2) under the control of the $p56^{lck}$ proximal promoter. In T cells from TSAd-SH2 TG mice, T cell receptor (TCR)-mediated early signaling events, such as $Ca^{2+}$ flux and ERK activation, were normal; however, late activation events, such as IL-2 production and proliferation, were significantly reduced. Moreover, TCR-induced cell adhesion to extracellular matrix (ECM) proteins and migration through ECM proteins were defective in T cells from TSAd-SH2 TG mice. Furthermore, the contact hypersensitivity (CHS) reaction, an inflammatory response mainly mediated by T helper 1 (Th1) cells, was inhibited in TSAd-SH2 TG mice. Taken together, these results show that TSAd, particularly the SH2 domain of TSAd, is essential for the effector functions of T cells.

• Molecules and Cells
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• v.40 no.5
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• pp.363-370
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• 2017

Extrahepatic cholangiocarcinoma (ECC), a malignant tumor of biliary origin, has a poor prognosis with limited treatment options. The KRAS oncogene is the most commonly mutated gene in ECC and one of the factors that predicts a poor prognosis and low survival rate. L1 cell adhesion molecule (L1CAM) is expressed in ECC cells and acts as an independent poor prognostic factor in predicting patient survival. In this study we investigate the functional significance of L1CAM in ECC cells with activating KRAS mutation. We selected an ECC cell line, EGI-1, with activating KRAS mutation, and then confirmed its expression of L1CAM by RT-PCR, western blot analysis, and flow cytometry. The suppression of L1CAM expression (using a specific lentivirus-delivered shRNA) significantly decreased the migratory and invasive properties of EGI-1 cells, without altering their proliferation or survival. Analyses of signaling effectors in L1CAM-depleted and control EGI-1 cells indicated that L1CAM suppression decreased the levels of both phosphorylated MKK4 and total MKK4, together with c-Jun N-terminal kinase (JNK) phosphorylation. Further, exposure to a JNK inhibitor (SP600125) decreased migration and invasion of EGI-1 cells. These results suggest that L1CAM promotes cellular migration and invasion via the induction of MKK4 expression, leading to JNK activation. Our study is the first to demonstrate a functional role for L1CAM in ECC carrying the activating KRAS mutation. Given that KRAS is the most commonly mutated oncogene in ECC, L1CAM may serve as an attractive therapeutic target for ECC cells with activating KRAS mutation.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.78-79
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• 2003

T cell activation is initited by the interaction of T cells with antigen-presenting cells (APCs) in the context of peptide antigen. Initial conjugates are formed by binding between lymphocyte-associated antigen-l (LFA-l, also known as CD11a-CD18) and intercellular adhesion molecule-l (ICAM-1), or CD2 and LFA-3, or other pairs of interactive proteins. (omitted)

• Reproductive and Developmental Biology
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• v.36 no.3
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• pp.155-161
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• 2012

Germ cell-specific hyaluronidases such as sperm adhesion molecule 1 (SPAM1) and hyaluronoglucosaminidase 5 (Hyal5) are in part responsible for dispersal of the cumulus cell mass, which is a critical step in establishing fertilization in mammals. In this study, we identified two testis-hyaluronidases, SPAM1 and Hyal5, in hamster and rat. These two genes were expressed specifically in the testis. At the protein level, hamster SPAM1 and Hyal5 display 78.7% and 75.4% identity with mouse SPAM1 and Hyal5. Further, the activity of the enzymes with respect to cumulus cell dispersion did not differ, although we observed that the enzymatic activity differed in pH range. These studies suggest that different sperm hyaluronidases are capable of dispersing the cumulus cell mass despite differences in enzyme activity.