• 제목/요약/키워드: Intercellular adhesion molecule-1 (ICAM-1)

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Phosphatidic acid에 의한 intercellular adhesion molecule-1 발현 조절에 관여한 MAPK와 PKC-${\delta}$의 역할 (THE ROLE OF MAPK AND PKC-${\delta}$ IN PHOSPHATIDIC ACID-MEDIATED INTERCELLULAR ADHESION MOLECULE-1 EXPRESSION)

  • 조우성;윤홍식;진병로;백석환
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제33권5호
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    • pp.445-454
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    • 2007
  • Background: Phosphatidic acid(PA), an important second messenger, is involved in inflammation. Notably, cell-cell interactions via adhesion molecules playa central role in inflammation. This thesis show that PA induces expression of intercellular adhesion molecule-1(ICAM-1) on macrophages and describe the signaling pathways. Materials and methods: Macrophages were cultured in the presence of 10% FBS and assayed cell to cell adhesion using HUVEC. For the gene and protein analysis, RT-PCR, Western blot and flow cytometry were performed. In addition, overexpressed cell lines for dominant negative PKC-${\delta}$ mutant established and tested their effect on the promoter activity and expression of ICAM-1 protein by PA. Results: PA-activated macrophages significantly increased adhering to human umbilical vein endothelial cell and this adhesion was mediated by ICAM-1. Pretreatment with rottlerin(PKC-${\delta}$ inhibitor) or expression of a dominant negative PKC-${\delta}$ mutant, but not Go6976(classical PKC-${\alpha}$ inhibitor) and myristoylated PKC-${\xi}$ inhibitor, attenuated PA-induced ICAM-1 expression. The p38 mitogen-activated protein kinase(MAPK) inhibitor blocked PA-induced ICAM-1 expression in contrast, ERK upstream inhibitor didn't block ICAM-1. Conclusion: These data suggest that PA-induced ICAM-1 expression and cell-cell adhesion in macrophages requires PKC-${\delta}$ activation and that PKC-${\delta}$ activation is triggers to sequential activation of p38 MAPK.

인체 특발성 폐섬유증에서 Intercellular Adhesion Molecule-1의 발현에 관한 연구 (Expression of Intercellular Adhesion Molecule-1 in Human Idiopathic Pulmonary Fibrosis)

  • 박성수;신동호;김태화;이동후;이정희;이중달
    • Tuberculosis and Respiratory Diseases
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    • 제40권2호
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    • pp.185-191
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    • 1993
  • 연구배경 : ICAM-1은 90 kD의 당단백으로서 ${\beta}_2$ integrin과 관계를 가지며, 특발성 폐섬유증의 병인론에 있어서 ICAM-1의 발현과 밀접한 관계가 있다고 보고되고 있다. 특발성 폐섬유종에 있어서 ICAM-1의 발현 정도는 상향조절된다. 특발성 폐섬유증에 있어서 ICAM-1의 발현 양상에 대한 보고는 드물다. 방법 : 본 연구는 특발성 폐섬유증에 있어서 ICAM-1의 발현 양상을 연구하고자 개흉폐생검으로 채취된 특발성 간질성 폐섬유증 3예의 6절편과 폐절제시 채취한 3예의 정상조직을 연구재료로 하여 ICAM-1의 단세포군항체를 이용하여 연역조직화학적 검색을 실시하였다. 결과 : ICAM-1은 3예의 정상조직의 기관지 상피세포나 폐포 세포에서는 발현되지 않았다. 3예의 특발성 폐섬유증 6절편 중 5절편에서 폐포벽의 간질성 섬유아 세포들에서 발현되었고, 1절편에서는 증식된 폐포내 폐포세포에서 발현되었다. 그 정도는 비균질적인 양상을 보였다. 3예의 6절편 중 5절편에서 강한 발현을 1절편에서는 약한 발현정도를 나타냈다. 결론 : 위의 연구 결과를 종합하여 보면, ICAM-1의 발현 증가는 특발성 폐섬유증의 병인과 상당한 관련이 있음을 암시해 주는 것으로 추정된다.

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HCMV에 감염된 TBP-1 세포에서 세포간 부착분자-1 발현 촉진물질의 방출 (Secretion of Cytokine Stimulating Intercellular Adhesion Molecule-l Expression from THP-l Cells Infected with Human Cytomegalovirus)

  • 김미숙;이현아;이찬희
    • 미생물학회지
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    • 제44권2호
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    • pp.140-146
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    • 2008
  • 다양한 염증 질환을 유발하는 사람세포거대바이러스(Human cytomegalovirus: HCMV)는 단핵구 세포주인 THP-1 세포에서 염증반응의 중요한 매개체인 세포간부착분자-1(intercellular adhesion molecule: ICAM-1) 발현을 촉진한다. ICAM-1 발현은 자외선으로 불활화시킨 HCMV (UV-HCMV)에 의해서도 촉진되므로 이 과정에 HCMV 유전자발현은 꼭 필요하지는 않은 것 같다. HCMV에 감염된 THP-1 세포 배양액을 감염되지 않은 THP-1 세포에 처리하거나 공유하게 하였을 시 감염되지 않은 세포에서도 ICAM-1 발현이 증가하였다. 감염된 세포 배양액에 의한 ICAM-1 발현 증가는 $NF-{\kappa}B$ 경로를 거친다. UV-HCMV에 감염된 세포의 배양액은 ICAM-1 발현을 촉진시키지 못하였다. 따라서 HCMV에 의한 THP-1 세포에서 ICAM-1 발현 증가는 바이러스 유전자 발현을 필요로 하지 않지만, 감염된 세포에서 ICAM-1 발현을 촉진하는 물질을 분비하는 과정에는 바이러스 유전자 발현이 필요한 것으로 생각된다.

진행된 구강암 및 후두암 환장의 혈청 Intercellular Adhesion Molecule-1(ICAM-1) 및 Sialic acid(SA)농도 (Levels of Soluble Intercelluar Adhesion Molecule-1 and Total Sialic Acid in Serum of Patients with Oral Cavity Cancer and Laryngeal Cancer)

  • 최승효;윤두환;강진욱;임현우;권현자;박정제;남순열
    • 대한기관식도과학회지
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    • 제10권1호
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    • pp.35-40
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    • 2004
  • Adhesion molecules have been implicated in tumor progression. In this study, we aimed to investigate serum soluble intercellular adhesion molecule-1 (ICAM-1) and sialic acid (SA) levels in oral cavity cancer and laryngeal cancer and correlate their levels with cancer progression. Method : The sera from 31 patients with advanced oral cavity cancer (5 at stage III, 10 at stage IV) and advanced laryngeal cancer (1 at stage III, 15 at stage IV) were extracted before treatment. The concentrations of ICAM-1 was measured by Endogen kit (measured absorbance at 490nm) and the concentration of SA was measured by Roche kit (measured absorbance at 550nm). Respectively, gained data was compared with those from a control group (n=12). Result : Mean serum ICAM-1 and SA levels were found to be higher in oral cavity cancer group and laryngeal cancer group than control group. But statistical meaning was at SA (p<0.001, oral cavity cancer and laryngeal cancer versus control). Conclusion : These data reveal that the significant correlations serum SA level in advanced oral cavity cancer and laryngeal cancer. Serum ICAM-1 level was higher at advanced oral cavity cancer and laryngeal cancer than at control group but that was not significant.

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

  • 전창덕
    • 한국동물학회:뉴스레터
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    • 제18권2호
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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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γ-Irradiation Induced Adhesion Molecules are Reduced by Vitamin C in Human Endothelial Cells

  • Son, Eun-Wha;Kim, Byung-Oh;Pyo, Suh-Kneung
    • Biomolecules & Therapeutics
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    • 제12권3호
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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.

Protein tyrosine phosphatase PTPN21 acts as a negative regulator of ICAM-1 by dephosphorylating IKKβ in TNF-α-stimulated human keratinocytes

  • Cho, Young-Chang;Kim, Ba Reum;Cho, Sayeon
    • BMB Reports
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    • 제50권11호
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    • pp.584-589
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    • 2017
  • Intercellular adhesion molecule-1 (ICAM-1), which is induced by tumor necrosis factor (TNF)-${\alpha}$, contributes to the entry of immune cells into the site of inflammation in the skin. Here, we show that protein tyrosine phosphatase non-receptor type 21 (PTPN21) negatively regulates ICAM-1 expression in human keratinocytes. PTPN21 expression was transiently induced after stimulation with TNF-${\alpha}$. When overexpressed, PTPN21 inhibited the expression of ICAM-1 in HaCaT cells but PTPN21 C1108S, a phosphatase activity-inactive mutant, failed to inhibit ICAM-1 expression. Nuclear factor-${\kappa}B$ (NF-${\kappa}B$), a key transcription factor of ICAM-1 gene expression, was inhibited by PTPN21, but not by PTPN21 C1108S. PTPN21 directly dephosphorylated phospho-inhibitor of ${\kappa}B$ ($I{\kappa}B$)-kinase ${\beta}$ ($IKK{\beta}$) at Ser177/181. This dephosphorylation led to the stabilization of $I{\kappa}B{\alpha}$ and inhibition of NF-${\kappa}B$ activity. Taken together, our results suggest that PTPN21 could be a valuable molecular target for regulation of inflammation in the skin by dephosphorylating p-$IKK{\beta}$ and inhibiting NF-${\kappa}B$ signaling.

The relationship between serum adiponectin and inflammatory cytokines in obese Korean juveniles

  • Byun, Sung Hwan;Kwon, Eun Byul;Kim, Se Young
    • Clinical and Experimental Pediatrics
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    • 제57권12호
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    • pp.533-537
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    • 2014
  • Purpose: Obesity is related to systemic inflammatory processes causing cardiovascular complications. Intercellular adhesion molecule-1 (ICAM-1), CD40 ligand (CD40L), P-selectin are newly described mediators of inflammation and have a significant effect in atherosclerosis. Adiponectin has shown anti-inflammatory effects in adults. The aim of this study was to evaluate the relationship between adiponectin and inflammatory mediators in children and adolescents. Methods: Fifty children or adolescents, twenty two with a body mass index (BMI) over 95th percentile, and twenty eight with a BMI below 75th percentile were included in the study. Serum soluble ICAM-1 (sICAM-1), P-selectin, CD40L, lipid profiles, aspartate aminotransferase, alanine aminotransferase, glucose and insulin were measured to evaluate associations with adiponectin. Comparison of these variables was performed between the obese and the nonobese group. Results: We found a adiponectin to be significant lower and sICAM-1 significant higher in the obese group compared to the nonobese group, but there were no significant differences in P-selectin and soluble CD40L. Adiponectin was negatively associated with ICAM-1 and P-selectin in the obese group. Conclusion: Negative associations of adiponectin with ICAM-1 and P-selectin in obese children and adolescents suggest that serum adiponectin level may represent the inflammatory status.

Gamma-irradiation induced expression of ICAM-l on human meuroblastoma cells is mediated by the activation of p38 MAP kinase.

  • Son, Eun-Hwa;Mo, Sung-Ji;Rhee, Dong-Kwon;Pyo, Suhk-Neung
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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    • pp.139.1-139.1
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    • 2003
  • Since radiotherapy has been suspected to promote tumor metastasis and the presence of increase levels of adhesion molecules have implications for metastasis, we decided to investigate whether gamma-irradiation alters the expression of intercellular adhesion molecule-1 (ICAM-1) on neuroblastoma cells and the activities of relevant intracellular signaling molecules. In the present study, the relative of ICAM-1 expression under gamma-irradiated neuroblastoma cells were assessed by Western blot analysis. (omitted)

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