• Korean Journal of Microbiology
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• v.44 no.2
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• pp.140-146
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• 2008

Human cytomegalovirus (HCMV) stimulates the expression of intercellular adhesion molecule (ICAM-l) on the surface of monocytic THP-1 cells. Stimulation of ICAM-l did not require HCMV gene expression since UV-inactivated HCMV (UV-HCMV) was able to induce ICAM-l expression. ICAM-l expression was also stimulated in uninfected THP-l cells which were fed with culture supernatant of HCMV-infected THP-l cells. Co-culture experiment using trans-well insert supported that HCMV-infected THP-l cells secreted some cytokine(s) stimulating ICAM-l expression. The stimulation of ICAM-l by HCMV-infected cell culture supernatant appears to involve $NF-{\kappa}B$ pathway. Culture supernatant from THP-l cells infected with UV-HCMV, whose gene expression was abrogated, failed to stimulate ICAM-l expression on naive THP-l cells. Thus, HCMV gene expression seems to be required in secretion of cytokine(s) stimulating ICAM-l expression.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.25 no.6
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• pp.441-452
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• 2022

Congenital diarrheal disorders (CDDs) with genetic etiology are uncommon hereditary intestinal diseases characterized by chronic, life-threatening, intractable watery diarrhea that starts in infancy. CDDs can be mechanistically divided into osmotic and secretory diarrhea. Congenital tufting enteropathy (CTE), also known as intestinal epithelial dysplasia, is a type of secretory CDD. CTE is a rare autosomal recessive enteropathy that presents with intractable neonatal-onset diarrhea, intestinal failure, severe malnutrition, and parenteral nutrition dependence. Villous atrophy of the intestinal epithelium, crypt hyperplasia, and irregularity of surface enterocytes are the specific pathological findings of CTE. The small intestine and occasionally the colonic mucosa include focal epithelial tufts. In 2008, Sivagnanam et al. discovered that mutations in the epithelial cell adhesion molecule (EpCAM, MIM# 185535) were the genetic cause of CTE (MIM# 613217). More than a hundred mutations have been reported to date. Furthermore, mutations in the serine peptidase inhibitor Kunitz type 2 (SPINT2, MIM# 605124) have been linked to syndromic CTE. In this study, we report the case of a 17-month-old male infant with congenital diarrhea. Despite extensive etiological workup, no etiology could be established before admission to our center. The patient died 15 hours after being admitted to our center in a metabolically decompensated state, probably due to a delay in admission and diagnosis. Molecular autopsy with exome sequencing revealed a previously reported homozygous missense variant, c.757G>A, in EpCAM, which was confirmed by histopathological examination.

• Proceedings of the PSK Conference
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• 2003.10b
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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)

• Tuberculosis and Respiratory Diseases
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• v.58 no.3
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• pp.276-284
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• 2005

Backgraound : There have been many reports on the pathogenesis of sepsis-induced acute respiratory distress syndrome(ARDS) but, the precise mechanism has not been elucidated. This study examined the protective effect of an inhibition of platelet activating factor(PAF) remodeling and the adhesion molecule on the oxidative stress of the lungs in rats with an endotoxin induced acute lung injury(ALI). Methods : ALI was induced in Sprague-Dawley rats by instilling an E-coli endotoxin into the trachea. Ketotifen and fucoidan were used respectively to inhibit PAF remodeling and adhesion molecule. The lung leak index, lung myeloperoxidase(MPO) activity, bronchoalveolar lavage(BAL) fluid neutrophil count and lyso PAF acetyltransferase activity(AT), were measured and an ultrastructural study and cytochemical electron microscopy were performed. Results : The lung leak index, lung MPO activity, BAL fluid neutrophil count and lyso PAF AT activity was higher in the endotoxin-treated rats. In addition, severe destruction of the pulmonary architecture and increased hydrogen peroxide production were identified. These changes were reversed by ketotifen. However, fucoidan did not appear to have any protective effects. Conclusion : The inhibition of PAF remodeling appeared to be effective in decreasing the endotoxin-induced ALI. In addition, this effect might be derived from the inhibition of neutrophilic oxidative stress. However, the inhibition of the adhesion molecules by fucoidan appeared to be ineffective in decreasing the endotoxin-induced ALI.

• Herbal Formula Science
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• v.20 no.1
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• pp.1-11
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• 2012

Objectives : This experimental study was designed to investigate the inhibitory effects of combination with Korean red ginseng and Gastrodia rhizoma on vascular dysfunction in high-fat/cholesterol diet-induced hyperlipidemia. Methods : Sprague-Dawley rats were fed with 7.5% cocoa butter and 1.25% cholesterol for 10 weeks, with Panax ginseng (PG), and mixtures of Panax ginseng and Gastrodia rhizoma (PGM), respectively. Results : Chronic treatment with PG and PGM significantly decreased body weight. The aortic expression of cell adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin were markedly increased in hyperlipidemia rats. Interestingly, PGM significantly decreased cell adhesion molecules expression. However, there was no significant decrease in PG group. In addition, PG and PGM group inhibited high-fat/cholesterol diet-induced cytokine such as monocyte chemoattractant protein (MCP-1) mRNA expression. Furthermore, PG and PGM group significantly decreased c-reactive protein protein (CRP) level. Especially, PGM significantly accentuated the decrease of MCP-1 mRNA expression and CRP level. Conclusions : the present study provides an evidence that combination with Panax ginseng and Gastrodia rhizoma enhances anti-vascular protective effects through suppression of vascular inflammation in hyperlipidemic rats.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.109-115
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• 2005

Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD(P)H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 ($3.5{\pm}0.4$) and VCAM-1 ($3.8{\pm}0.3$) in diabetic aorta was significantly higher than those in control aorta ($0.9{\pm}0.5$ and $1.6{\pm}0.3$, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD(P)H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P＜0.01 in ICAM-1 and r=0.88, P＜0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD(P)H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.5
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• pp.1132-1138
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• 2009

Vascular inflammation is an important event in the development of vascular diseases such as tumor progression and atherosclerosis. This study was to investigate the inhibitory effects of WK-38, a new herbal prescription for the treatment of atherosclerosis, on vascular inflammation in human umbilical vein endothelial cells (HUVEC). WK-38 is composed of Rhei Rhizoma, Magonoliae Cortex, Moutan Cortez Radicis. Pretreatment with WK-38 was significantly blocked TNF-$\alpha$-induced expression level of cell adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), and endothelial cell selectin (E-selectin) in a dose-dependent manner. TNF-$\alpha$-induced cell adhesion in co-cultured U937 and HUVEC was also blocked by pretreatment with WK-38. Moreover, WK-38 significantly suppressed p65 NF-${\kappa}B$ translocation into the nucleus by TNF-$\alpha$ as well as the phosphorylation and degradation of $I{\kappa}B-{\alpha}$. In conclusion, the present data suggested that WK-38 could suppress TNF-$\alpha$-induced vascular inflammatory process, though inhibition of NF-${\kappa}B$ activation in HUVEC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.31 no.1
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• pp.1-6
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• 2005

It becomes more concerned that the cell adhesion molecule plays an important role in the process of malignant transformation and tumor behaviors including invasive growth and metastasis. It is postulated if the expression of adhesion molecule is reduced in tumor tissue, the tumor cell will be undifferentiated and lose their cell adhesion ability and polarity. So the tumor cells lost the adhesion of cell to cell and to basement membrane that they became more aggressive. Reduced cadherin expression enhances invasiveness through infiltrative growth and metastasis of tumor cells is well known and mostly accepted in many epithelia tumors. We explored the expression of E-cadherin by immunohistochemical staining in 50 oral squamous cell carcinomas and investigated the correlation between the expression of E-cadherin and clinicopathologic parameters and prognosis. The expression of E-cadherin was reduced in 40/50(80%) of primary tumors, and 21/22(95.5%) of lymph nodes. The reduced expression of the E-cadherin was associated with lymph node metastasis(P=0.029), invasive mode(P=0.030) and marginal status(P=0.038). Survival analysis showed that predictive period of E-cadherin reduced group(37 months) was lower than that of E-cadherin preserved group(60 months), but there was no statistical significant difference.

• International Journal of Stem Cells
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• v.17 no.1
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• pp.70-79
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• 2024

The efficacy of adipose-derived stem cells (ASCs) on myocardial infarction is limited due to poor survival and engraftment. Integrin-mediated cell adhesion is a prerequisite for its survival and homing. ASCs expressed insufficient integrin 𝛼₄, limiting their homing capacity. This study aims to characterize integrin 𝛼₄⁺ ASC subpopulation and investigate their therapeutic efficacy in myocardial infarction. We used fluorescence-activated cell sorting to harvest integrin 𝛼₄⁺ ASCs subpopulation, which were characterized in vitro and transplanted into myocardial infarction model. Positron emission tomography imaging were performed to measure infarction size. Cardiac cine magnetic resonance imaging was used to evaluate heart contractile function. Compared with the unfractionated ASCs, integrin 𝛼₄⁺ ASCs subpopulation secreted a higher level of angiogenic growth factors, migrated more rapidly, and exhibited a stronger anti-apoptotic capacity. Vascular cell adhesion molecule-1 was obviously up-regulated at 3 days after myocardial infarction, which interacted with integrin α₄ receptor on the surface of ASCs to enhance the survival and adhesion. Thus, we implanted unfractionated ASCs or integrin α₄⁺ ASCs subpopulation into the 3-day infarcted myocardium. Integrin α₄⁺ ASCs subpopulation exhibited more robust engraftment into the infarcted myocardium. Integrin α₄⁺ ASCs subpopulation more effectively decreased infarct size and strengthen cardiac function recovery than did the unfractionated ASCs. Integrin α₄⁺ ASCs subpopulation is superior to unfractionated ASCs in ameliorating ischemic myocardial damage in animal model. Mechanistically, their more robust engraftment into the infarct area, higher migratory capacity and their increased release of paracrine factors contribute to enhanced tissue repair.

• Toxicological Research
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• v.13 no.1_2
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• pp.1-21
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• 1997

염증반응이란 우리 신체에 외부 물질이 침입했을 경우 대처하는 정상적인 현상이다. 외부에서 물리, 화학, 생물학적 물질에 노출되었을 경우 혈관이 팽창하고, 비특이적 면역반응이 시작된다. Selectin, integrin, immunoglobulin superfamily와 같은 adhesion molecule에 의해 macrophage 및 neutrophil과 같은 leukocyte의 반응을 촉진하기 위해 exudation이 일어나고 침입 부위에 모여 hyperemia가 발생된다.(Govan 등, 1995)