• Title/Summary/Keyword: Adhesion molecule

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Anti-inflammatory Effect of Evodia Officinalis $D_{ODE}$ in Mouse Macrophage and Human Vascular Endotherial Cells (마우스 대식세포 및 사람 혈관 내피세포에서 오수유(Evodia officinalis $D_{ODE}$) 메탄올 추출물의 항염증 효과)

  • Yun, Hyun-Jeung;Heo, Sook-Kyoung;Lee, Young-Tae;Park, Won-Hwan;Park, Sun-Dong
    • The Korea Journal of Herbology
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    • v.23 no.1
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    • pp.29-38
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    • 2008
  • Objectives : Evodia officinalis DODE (EO), an herbal plant, has been widely used in traditional Korean medicine for the treatment of vascular diseases such as hypertension. The crude extract of EO contains phenolic compounds that are effective in protecting liver microsomes, hepatocytes, and erythrocytes against oxidative damage. But EO has been little found to have an anti-inflammatory activity. We investigated anti-inflammatory activity of EO in RAW 264.7 cells and human umbilical vein endothelial cells (HUVECs). Methods : Cytotoxic activity of EO on RAW 264.7 cells was investigated by using 5-(3-caroboxymeth-oxyphenyl)-2H-tetra-zolium inner salt (MTS) assay. The nitric oxide (NO) production was measured by Griess reagent system. And proinflammatory cytokines were measured by ELISA kit. The levels of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression were measured by flow cytometer. Results : EO decreased LPS-induced NO production in RAW 264.7 cells. The inhibitory activity of EO on LPS-induced NO release is probably associated with suppressing TNF-${\alpha}$, IL-6 and MCP-1 formation. These results indicate that EO has potential as an anti-inflammatory agent. Moreover, EO decreased TNF-${\alpha}$-induced IL-8, IL-6 production, and ICAM-1 and VCAM-1 expression in HUVECs. Conclusions : EO inhibits TNF-${\alpha}$-induced inflammation via decreasing cytokines production and adhesion molecules expression. These results indicate that EO has potential as an anti-inflammation and anti-artherosclerosis agent.

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Association between the simultaneous decrease in the levels of soluble vascular cell adhesion molecule-1 and S100 protein and good neurological outcomes in cardiac arrest survivors

  • Kim, Min-Jung;Kim, Taegyun;Suh, Gil Joon;Kwon, Woon Yong;Kim, Kyung Su;Jung, Yoon Sun;Ko, Jung-In;Shin, So Mi;Lee, A Reum
    • Clinical and Experimental Emergency Medicine
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    • v.5 no.4
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    • pp.211-218
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    • 2018
  • Objective This study aimed to determine whether simultaneous decreases in the serum levels of cell adhesion molecules (intracellular cell adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], and E-selectin) and S100 proteins within the first 24 hours after the return of spontaneous circulation were associated with good neurological outcomes in cardiac arrest survivors. Methods This retrospective observational study was based on prospectively collected data from a single emergency intensive care unit (ICU). Twenty-nine out-of-hospital cardiac arrest survivors who were admitted to the ICU for post-resuscitation care were enrolled. Blood samples were collected at 0 and 24 hours after ICU admission. According to the 6-month cerebral performance category (CPC) scale, the patients were divided into good (CPC 1 and 2, n=12) and poor (CPC 3 to 5, n=17) outcome groups. Results No difference was observed between the two groups in terms of the serum levels of ICAM-1, VCAM-1, E-selectin, and S100 at 0 and 24 hours. A simultaneous decrease in the serum levels of VCAM-1 and S100 as well as E-selectin and S100 was associated with good neurological outcomes. When other variables were adjusted, a simultaneous decrease in the serum levels of VCAM-1 and S100 was independently associated with good neurological outcomes (odds ratio, 9.285; 95% confidence interval, 1.073 to 80.318; P=0.043). Conclusion A simultaneous decrease in the serum levels of soluble VCAM-1 and S100 within the first 24 hours after the return of spontaneous circulation was associated with a good neurological outcome in out-of-hospital cardiac arrest survivors.

Anti-Angiogenic and Anti-Cell Adhesion Effect of the Camellia japonica Flower Extract (동백꽃 추출물의 신생혈관생성 및 세포부착 억제 효과)

  • Heo, In-Do;Seo, Hyo-Jin;Kim, Jong-Deog
    • 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.

Modulatory Effect of BAY11-7082 on CD29-mediated Cell-cell Adhesion in Monocytic U937 Cells (BAY11-7082에 의한 U937 세포의 CD29-매개성 세포간 유착과정 조절 효과)

  • Kim, Byung-Hun;Cho, Jae-Youl
    • YAKHAK HOEJI
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    • v.52 no.5
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    • pp.412-417
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    • 2008
  • BAY11-7082 was initially found to be an anti-inflammatory drug with NF-${\kappa}B$ inhibitory property. In this study, we evaluated modulatory function of BAY11-7082 on U937 cell-cell adhesion induced by CD29 (${\beta}1$-integrins). BAY11-7082 strongly blocked functional activation of CD29 (${\beta}1$-integrins), as assessed by cell-cell adhesion assay. However, this compound did not block a simple activation of CD29, as assessed by cell-fibronectin adhesion assay. In particular, to understand molecular mechanism of BAY11-7082-mediated inhibition, the regulatory roles of CD29-induced actin cytoskeleton rearrangement under cell-cell adhesion and surface level of CD29 were examined using confocal and flow cytometic analysis. Interestingly, this compound strongly suppressed the molecular association of actin cytoskeleton with CD29 at cell-cell adhesion site. Moreover, BAY11-7082 also diminished surface levels of CD29 as well as its-associated adhesion molecule CD147, but not other adhesion molecules such as CD18 and CD43. Therefore, our data suggest that BAY11-7082 may be involved in regulating immune responses managed by CD29-mediated cell-cell adhesion.

Fusobacterium nucleatum GroEL signaling via Toll-like receptor 4 in human microvascular endothelial cells

  • Lee, Hae-Ri;Choi, Bong-Kyu
    • International Journal of Oral Biology
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    • v.37 no.3
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    • pp.130-136
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    • 2012
  • The GroEL heat-shock protein from Fusobacterium nucleatum, a periodontopathogen, activates risk factors for atherosclerosis in human microvascular endothelial cells (HMEC-1) and ApoE-/- mice. In this study, we analyzed the signaling pathways by which F. nucleatum GroEL induces the proinflammatory factors in HMEC-1 cells known to be risk factors associated with the development of atherosclerosis and identified the cellular receptor used by GroEL. The MAPK and NF-${\kappa}B$ signaling pathways were found to be activated by GroEL to induce the expression of interleukin-8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and tissue factor (TF). These effects were inhibited by a TLR4 knockdown. Our results thus indicate that TLR4 is a key receptor that mediates the interaction of F. nucleatum GroEL with HMEC-1 cells and subsequently induces an inflammatory response via the MAPK and NF-${\kappa}B$ pathways.

Intercellular Adhesion Molecule-1 (ICAM-1)의 분자구조와 기능

  • 전창덕
    • The Zoological Society Korea : Newsletter
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    • v.18 no.2
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    • pp.33-37
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    • 2001
  • Intercellular adhesion molecule-1 (ICAM-1)은 T 세포의 활성이나 면역세포가 염증작용이 일어나고 있는 곳으로 옮겨갈 때 중요한 역할을 수행하는 당단백질 (glycoprotein)으로서 2-integrin 계열의 분자인 leukocyte function associated antigen-1(LFA-1)이나 Mac-1의 수용체이며 세포의 막에 homodimer인 상태로 발현되어진다. ICAM-1은 5개의 세포외 domain과 transmembrane domain(TM) 및 짧은 cytoplasmic domain을 갖고 있으며, dimerization motif는 domain 5 또는 TM인 것으로 알려져 있다. 최근의 crystal 구조분석 결과에 의하면 domain 1에도 dimerization motif가 있는 것으로 추정되어지지만 정확한 실험적인 뒷받침이 되어져 있지 않다. 본 연구에서는domain 1에 dimer를 형성할 수 있는 motif가 존재하는 지에 대한 실험적인 증명과 함께 ICAM-1이 세포의 막에서 어떠한 구조를 갖고 있는지에 대한 최근의 연구성과를 보고하고자 한다.

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