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Cardiotrophin-1 induces intercellular adhesion molecule-1 expression by nuclear factor κB activation in human umbilical vein endothelial cells

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Chinese Medical Journal 2008年第24期121卷 2592-2598页

作者： Michael Fritzenwanger Martin Foerster Katharina Meusel Christian Jung Hans R. Figulla Department of Internal Medicine I Friedrich-Schiller-University Jena Erlanger Allee 101 07740 Jena Germany

Background In addition to elevated concentrations of cytokines, patients with congestive endothelial dysfunction and increased plasma concentrations of adhesion molecules heart failure （CHF） show ke intercellular adhesion molecule-1 （ICAM-1）. Furthermore, the concentration of cardiotrophin-1 （CT-1） - a cytokine of the interleukin-6 superfamily - is increased in CHF. We tested the hypothesis whether CT-1 is able to induce ICAM-1 in human umbilical vein endothelial cells （HUVEC）. Furthermore we examined the signalling mechanisms of CT-1 mediated ICAM-1 expression. Methods Confluent layers of HUVEC were incubated with increasing concentrations of CT-1 （5 to 100 ng/ml） for different periods. ICAM-1 mRNA was determined by real-time polymerase chain reaction （PCR） and ICAM-1 surface expression by fluorescence-activated cell sorter （FACS） analysis and soluble ICAM-1 （slCAM-1） in the culture supernatant by enzyme linked immunosorbent assay （ELISA）. To clarify the signalling pathway of CT-1 induced ICAM-1 expression we used various inhibitors of possible signal transducing molecules, electromobility shift assay （EMSA） and Western blot analysis. Results CT-1 induced ICAM-1 mRNA （1.8±0.8 fold increase compared to unstimulated cells after 6 hours） and protein （1.4±0.2 fold increase compared to unstimulated cells after 48 hours） in HUVEC in a time- and concentration-dependent manner. EMSA experiments show that CT-1 causes nuclear factor （NF） κB activation. Because parthenolide could inhibit CT-1 induced ICAM-1 expression NFκB activation is required in this pathway. CT-1 did not activate extracellular signal regulated kinases （ERK）, c-Jun N-terminal kinase （JNK） and p38. Conclusion CT-1 is able to induce ICAM-1 in endothelial cells by NFκB activation. These results may explain in part elevated ICAM-1 concentrations in patients with CHF and endothelial dysfunction.

关键词： cardiotrophin-1 intercellular adhesion molecule-1 nuclear factor κB human umbilical vein endothelial cells

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Soluble intercellular adhesion molecule-1,D-lactate and diamine oxidase in patients with inflammatory bowel disease

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World Journal of Gastroenterology 2009年第31期15卷 3916-3919页

作者： Wei-Bing Song Yong-Hui Lv Zhen-Shu Zhang Ya-Nan Li Li-Ping Xiao Xin-Pei Yu Yuan-Yuan Wang Hong-Li Ji Li Ma Department of Gerontology Guangzhou General Hospital of the PLA Guangzhou 510010 Guangdong Province China The Traditional Chinese'Medical Hospital of Guangzhou City Guangzhou 510010 Guangdong Province China Institute for Digestive Diseases Nanfang Hospital Southern Medical University Guangzhou 510515 Guangdong Province China Suzhou River Cadre's Sanatorium Second Artillery Rest of the Cadres of the PLA Beijing 100086 China

AIM： To study the levels of serum soluble intercellular adhesion molecule-1 （sICAM-1）, plasma D-lactate and diamine oxidase （DAO） in patients with inflammatory bowel disease （IBD）, and the potential clinical significance. METHODS： Sixty-nine patients with IBD and 30 healthy controls were included in this study. The concentration of sICAM-1 was detected with enzyme-linked immunosorbent assay, the level of D-lactate and DAO was measured by spectroscopic analysis, and the number of white blood cells （WBC） was determined by routine procedure. RESULTS： The levels of sICAM-I, DAO, and WBC in IBD patients were significantly higher than those in the control group （P 〈 0,01）, sICAM-I in IBD patients was found to be closely related to the levels of DAO and D-lactate （212.94 ± 69.89 vs 6.35 ± 2.35, P = 0.000）, DAO 212.94 ± 69.89 vs 8.65 ± 3.54, P = 0.000） and WBC （212.94 ± 69.89 vs 7.40 ± 2.61, P = 0.000）, but no significant difference was observed between patients with ulcerative colitis and patients with Crohn＇s disease. The post-treatment levels of sICAM-I, D-lactate and WBC were significantly lower than before treatment （sICAM-I 206.57 ± 79.21 vs 146.21 ± 64.43, P = 0.000）, （D-lactate 1.46 ± 0.94 vs 0.52± 0.32, P = 0.000） and （WBC 7.24 ± 0.2.33 vs 5.21 ± 3.21, P = 0.000）. CONCLUSION： sICAM-1, D-lactate and DAO are closely related to the specific conditions of IBD, and thus could be used as a major diagnostic index.

关键词： Inflammatory bowel diseases intercellular adhesion molecule-1 D-lactate Diamine oxidase

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Up-regulation of intestinal nuclear factor kappa B and intercellular adhesion molecule-1 following traumatic brain injury in rats

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World Journal of Gastroenterology 2005年第8期11卷 1149-1154页

作者： Chun-HuaHang Ji-XinShi Jie-ShouLi Wei-QinLi Hong-XiaYin DepartmentofNeurosurgery JinlingHospitalClinicalSchoolofMedicineNanjingUniversityNanjing210002JiangsuProvinceChina ResearchInstituteofGeneralSurgery JinlingHospitalClinicalSchoolofMedicineNanjingUniversityNanjing210002JiangsuProvinceChina

AIM: Nuclear factor kappa B (NF-κB) regulates a large number of genes involved in the inflammatory response to critical illnesses, but it is not known if and how NF-KB is activated and intercellular adhesion molecule-1 (ICAM-1) expressed in the gut following traumatic brain injury (TBI). The aim of current study was to investigate the temporal pattern of intestinal NF-κB activation and ICAM-1 expression following TBI. METHODS: Male Wistar rats were randomly divided into six groups (6 rats in each group) including controls with sham operation and TBI groups at hours 3, 12, 24, and 72, and on d 7. Parietal brain contusion was adopted using weight-dropping method. All rats were decapitated at corresponding time point and mid-jejunum samples were taken. NF-KB binding activity in jejunal tissue was measured using EMSA. Immunohistochemistry was used for detection of ICAM-1 expression in jejunal samples. RESULTS: There was a very low NF-κB binding activity and little ICAM-1 expression in the gut of control rats after sham surgery. NF-KB binding activity in jejunum significantly increased by 160% at 3 h following TBI (P1 was significantly up-regulated on the endothelia of microvessels in villous interstitium and lamina propria by 24 h following TBI and maximally expressed at 72 h post-injury (P1). The endothelial ICAM-1 immunoreactivity in jejunal mucosa still remained strong on d 7 post-injury. The peak of NF-κB activation and endothelial ICAM-1 expression coincided in time with the period during which secondary mucosal injury of the gut was also at their culmination following TBI. CONCLUSION: TBI could induce an immediate and persistent up-regulation of NF-κB activity and subsequent up-regulation of ICAM-1 expression in the intestine. Inflammatory response mediated by increased NF-κB activation and ICAM-1 expression may play an impor

关键词： Traumatic brain injury Intestine Nuclear factor kappa B intercellular adhesion molecule-1 Inflammatory response

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Polymorphism K469E of intercellular adhesion molecule-1 gene and restenosis after coronary stenting in Chinese patients

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Chinese Medical Journal 2004年第2期17卷 172-175页

作者：刘兆平霍勇李建平张岩薛琳赵春玉洪秀梅黄爱群高炜 Department of Cardiology First Hospital of Peking University Beijing 100034 China Anhui Province Biomedical Institution Hefei 230032 China Bioscience Department University of Science and Technology of China Hefei 230026 China

Background Inflammation is a major cause of restenosis after coronary stenting. intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule that plays a key role in the tight adhesion between leukocytes and vascular endothelium. The object of this study was to investigate the association between the K469E polymorphism of the ICAM-1 gene and restenosis after coronary stenting in North Chinese population.Methods The ICAM-1 K469E polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism method in 124 patients who had undergone coronary stenting and coronary angiography at least 3 months earlier. Information on clinical risk factors and procedure-related data were also collected.Results Of 124 enrolled patients in total, there were 72 cases of in-stent restenosis. The restenosis rate in this population was 58.1 %. The frequencies of the three possible genotypes of the ICAM-1 K469E polymorphism were: KK genotype 50. 8%, EE genotype 41. 9%, and EK genotype 41. 9%. Among restenosis patients, the frequency of the KK genotype was 58. 3% and the frequency of E allele carriers was 41.7%. Among non-restenosis patients, the frequency of the KK genotype was 40.4%, and the frequency of E allele carriers was 59. 6%. The distribution of these two genotype groups between restenosis and non-restenosis patients was significantly different (P=0. 049). Using multivariate logistic regression, the difference between the two groups was more apparent. The odds ratio of KK homozygotes vs E allele carriers was 2. 6, with 95% confidence interval 1. 2 -5. 8 ( P = 0. 018). After grading of risk factors, we found that the KK genotype was a stronger predictor of in-stent restenosis in obesity or hyperlipemia patients, with an odds ratio of 9. 3 and 3. 7, respectively (P <0. 05).Conclusion In our study population, KK homozygotes of the ICAM-1 codon 469 mutation had a higher risk of restenosis after coronary sten

关键词： coronary diseases intercellular adhesion molecule-1 gene polymorphism stents restenosis

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Mild hypothermia effects on intercellular adhesion molecule-1 and serum interleukin-6 expression in brain tissues of a rat focal ischemia model

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Neural Regeneration Research 2008年第10期3卷 1124-1127页

作者： Shengqi Fu Lei Yang Shuling Zhang Shilong Sun Xingai Mao Department of Neurology Fifth People＇s Hospital of Zhengzhou 450003 He＇nan Province China Department of Emergency He＇nan People＇s Hospital Zhengzhou 450003 He＇nan Province China Department of Neurology First Affiliated Hospital Xinxiang Medical College Weihui 453100 He＇nan Province China

BACKGROUND： Previous studies have confirmed the neuroprotective effect of mild hypothermia on ischemic brain injury. OBJECTIVE： To investigate the effects of mild hypothermia on intercellular adhesion molecule-1 expression and serum interleukin-6 levels in ischemic brain tissues of focal brain ischemia rats, and to explore the neuroprotective effects of mild hypothermia on ischemic brain injury. DESIGN, TIME AND SETTING： A randomized, controlled, neurobiological experiment was performed at the Central Laboratory, First Affiliated Hospital, Xinxiang Medical College, China from February to July 2006. MATERIALS： Thirty healthy, adult, Sprague Dawley rats were used to establish middle cerebral artery occlusion models using the suture method, The immunohistochemistry （streptavidin-biotin-peroxidase complex method） kit was purchased from Boster, China. Interleukin-6 radioimmunoassay was supplied by Institute of Radioimmunity, Technology Development Center, General Hospital of Chinese PLA. METHODS： The rats were equally and randomly assigned into mild hypothermia and control groups, and middle cerebral artery occlusion models were established. The rectal temperature was maintained at （37 ±0.5）℃ in the control group. In the mild hypothermia group, the rectal temperature was maintained at （33±1）℃. MAIN OUTCOME MEASURES： At 12 hours after model establishment, the ischemic brain hemispheres were coronally sliced at the level of the optic chiasm. The number of intercellular adhesion molecule-1-positive vessels per high-power field was observed with an optical microscope. Serum interleukin-6 levels were measured by radioimmunoassay. RESULTS： Compared with the control group, intercellular adhesion molecule-1 and serum interleukin-6 expressions were significantly decreased in ischemic brain tissues of the mild hypothermia group （P 〈 0.01）. CONCLUSION： Mild hypothermia exhibits a neuroprotective effect by reducing serum interleukin-6 and intercellular adhesion molecule-1 expression

关键词： cerebral ischemia intercellular adhesion molecule-1 interleukin-6 mild hypothermia

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Increased expression of intercellular adhesion molecule-1 in mouse focal cerebral ischemia model

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Chinese Medical Journal 2000年第1期113卷 75-79页

作者：葛海良 Institute of Shanghai Immunology Shanghai Second Medical University Shanghai 200025 China Institute of Shanghai Immunology Shanghai Second Medical University 280 South Chongqing Road Shanghai 200025 China Department of Surgery (Neurosurgery) University of Michigan Ann Arbor MI 48109 United States

OBJECTIVE: To quantitatively measure the temporal profiles of intercellular adhesion molecule-1 (ICAM-1) protein in mouse brain after middle cerebral artery occlusion (MCAO). METHODS: Adult male CD-1 mice received 0, 3, 6, 12, 24, 48 and 72 hour(s) of permanent MCAO with an intraluminal suture technique. The degree and the extent of occlusion were determined using a laser Doppler flowmeter. ICAM-1 positive expression in ischemic regions was determined immunohistochemically and ICAM-1 protein was quantitatively measured using immunoprecipitation and Western blot analysis. RESULTS: After MCAO, surface cerebral blood flow (CBF) in the ischemic hemisphere decreased to 9%-15% of the baseline in each time point of 7 to 8 animals. There were no significant differences in CBF measurement during occlusion between groups. Immunohistochemistry showed that ICAM-1 positive microvascular endothelial cells were observed both in the ischemic core and in the perifocal region. There was a tendency for increasing expression of ICAM-1 positive microvascular endothelial cells from the ischemic core to the ischemic margin. Western blot analysis showed that ICAM-1 expression in the ischemic hemisphere began to increase 3 h after MCAO, peaked at 6 h to 12 h, and persisted to 72 h. CONCLUSIONS: ICAM-1 expression increases in mice with permanent MCAO because ICAM-1 can mediate leukocyte-endothelial adhesion and progression of leukocyte infiltration after permanent focal cerebral ischemia. ICAM-1 is one of the important factors participating in ischemic cerebral damage and pathogenesis of stroke.

关键词： Animals Blotting, Western Brain Ischemia Immunohistochemistry intercellular adhesion molecule-1 Male Mice

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The Value of the Soluable intercellular adhesion molecule-1 Levels in Matermal Serum for Determination of Occult Chorioamnionitis in Premature Rupture of Membranes

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第2期24卷 154-157页

作者：邹丽张会军祝建芳朱剑文 Department of Obstetrics and Gynecology Union Hospital Tongji Medical College Huazhong University of Science and Technology Department of Obstetrics and Gynecology Shougang Hospital Beijing Universigy

To compare the diagnostic value of soluble intercellular adhesion molecule 1 (sICAM-1) with that of c-reactive protein (CRP) for detecting chorioamnionitis (CAM) in serum of women with premature rupture of membranes (PROM), 55 pregnant women with PROM, including 18 pregnant women with preterm premature rupture of membranes (PPROM) and 20 normal pregnant women at term (TPROM) were studied. Maternal serum were measured by Sandwish enzyme-linked immunoabsorbent assay (ELISA) for sICAM. CAM was histologically confirmed after delivery. The results revealed that (1) maternal serum levels of sICAM-1 and CRP were significantly higher in women with PROM than those without it; (2) maternal serum levels of sICAM-1 and CRP were significantly higher in women with CAM than those without it; (3) serum levels of sICAM-1 in PPROM women were similar to those in TPROM women, whereas serum levels of CRP in PPROM women were significantly higher than those in TPROM women; (4) the sensitivity, specificity, positive predictive value, negative predictive value, Kappa index and area under receiver operating characteristic (ROC) curve of maternal serum sICAM-1 (cutoff 104.7 ng/ml) and CRP(cutoff 1.03 mg/dl) for diagnosing CAM were 100 %, 91.2 %, 87.5 %, 100 %, 0.20, 0.995 and 81.0 %, 73.5 %, 65.4 %, 86.2 %, 0.13, 0.811, respectively; (5) among the mild histological CAM group, severe histological CAM group and clinical CAM group, the difference in maternal serum levels of sICAM-1 were significantly (P<0.001), with the order of concentration from high level to low level corresponding to the severity of CAM. It is concluded that maternal serum level of ICAM-1 is superior to that of CRP as biomarker for diagnosing intraamniotic infection in pregnant women with PROM.

关键词： intercellular adhesion molecule-1 chorioamninitis diagnosis

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Inhibitors of 5-lipoxygenase inhibit expression of intercellular adhesion molecule-1 in human melanoma cells

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Acta Pharmacologica Sinica 2004年第5期 130-135页

作者： Yin WANG2, Bin ZHOU, Ji LI2, Yong-bing CAO, Xin-sheng CHEN, Ming-he CHENG, Ming YIN3, 4Department of Pharmacology, School of Pharmacy, Second Military Medical University, Shanghai 200433, China 2No 455 Hospital of PLA, Shanghai 200336 3School of Pharmacy, Shanghai Jiaotong University, Shanghai 200030, China

AIM: To study the effect of 5-lipoxygenase inhibitors on the expression of intercellular adhesion molecule-1 (ICAM-1) inmelanoma cells. METHODS: ICAM-1 protein of human melanoma cell a375 was detected by enzyme-linkedimmunosorbent, flow cytometry and Western blot analysis. Level of ICAM-1 mRNA in a375 was evaluated byNorthern blot analysis. adhesion of a375 to endothelial cell EC304 was analyzed by isotopic tracing. RESULTS:5-Lipoxygenase inhibitors nordihydroguaiaretic acid, AA861 and MK886, could suppress the expression of ICAM-1protein as well as of its mRNA in a375 cells and reduce the adhesion of a375 to EC304. CONCLUSION:5-Lipoxygenase inhibitors can inhibit the expression of ICAM-1 in human melanoma cells and may be valuable fortreatment of melanoma metastasis.

关键词： lipoxygenase inhibitors intercellular adhesion molecule-1 adhesions melanoma metastasis

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Expression of intercellular adhesion molecule-1 in U937 foam cells and the inhibitory effect of imperatorin

Expression of intercellular adhesion molecule-1 in U937 foam...

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2002全国青年药理学英文学术会议

作者： YANG Peng-yuan, RUI Yao-cheng, LI Tie-jun(Department of Pharmacology, School of Pharmacy, The Second Medical MilitaryUniversity, Shanghai 200433,China)

AIM: To investigate the expression level of ICAM-1 in a macrophage-derived foam cell model from human U937 cell line. With a further study on the inflammatory reactions during the process of atherosclerosis, the inhibitory effect of imperatorin (IMP) was determined. METHOD: U937 cells were incubated with 80mg/L oxidized low density lipoprotein (ox-LDL) for 48 hours and a macrophage-derived foam cell model was established. The medium was pretreated with different concentration of IMP (0,25,50,100μmol/L). ICAM-1 protein expression in cells was measured with western blot;ICAM-1

关键词： foam cells intercellular adhesion molecule-1 imperatorin oxidized low density lipoprotein western blot northern blot

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Influence of glycated low density lipoprotein on the proliferation, expression of intercellular adhesion molecule-l, von Willebrand factor of human umbilical endothelial cells

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Chinese Medical Journal 2009年第21期122卷 2662-2665页

作者： LU Jun LIU Hui-ying ZHANG Xiu-zhen LEI Tao Department of Endocrinology and Metabolism Gongli Hospital Shanghai 200135 China Department of Endocrinology and Metabolism Tongji Hospital of Tongji University Shanghai 200065 China

Diabetes mellitus known as its macro- and microangiopathy has caused thousands of mortality per year. Recent researches showed that hyperglycemia, advanced glycation end products （AGEs） and some other factors acted on the process of atherogenesis. AGEs can combine with receptors of AGEs （RAGEs）, which exist on the vascular endothelium, smooth muscle cells, macrophage, lymphocyte and so on. They can stimulate series of signal transduction systems including nuclear factor κB （NF-κB） pathway, finally promote the secretion of inflammatory factor such as interleukin-1 （IL-1）, interleukin-6 （IL-6）, tumor necrosis factor-α （TNF-α）, intercellular adhesion molecule-1 （ICAM-1）,1＇2 as well as increase the synthesis and secretion of coagulant modulatory factors such as vascular cell adhesion molecule- 1 （VCAM- 1） and von Willebrand factor （vWF）.3

关键词： low density lipoprotein von Willebrand factor intercellular adhesion molecule-1

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