To investigate the pathogenesis of accelerated graft atherosclerosis after rdiac transplantation, a genetically well-defined and reproducible animal del is required. We performed heterotopic intraabdominal heart transplantation tween the two inbred strains of mice. Forty hearts from B10.A mice were ansplanted into B10.BR mice. Recipients were sacrificed at 1, 3, 5, 7, 14, 28, d 42 days after implantation. The specimens from both donor and recipient were amined with fluorescent immunohistochemistry and the serial histopathologic anges were evaluated. In the donor hearts, ICAM-1 and VCAM-1 expressions were nimal at day 1 and they gradually increased, reaching their peaks on day 5 or and remained unchanged by day 42. However, there were very little expressions the recipients' hearts. Mean percent areas of intima in the donor coronaries vealed progressive increase by day 42. However, those in the recipients cupied consistently less than 5% of the lumen. In conclusion, we demonstrated at a heterotopic murine heart transplantation model was a useful tool to oduce transplantation coronary artery disease and that adhesion molecules on e cardiac allografts were activated very early and remained elevated at all me-points, nonetheless the arterial lesion was detected after day 28 and its ogression was accelerated thereafter.
Animal ; Coronary Vessels/pathology ; Heart Transplantation*/pathology ; Intercellular Adhesion Molecule-1/biosynthesis* ; Mice ; Myocardium/pathology ; Myocardium/metabolism* ; Time Factors ; Transplantation, Heterotopic*/pathology ; Vascular Cell Adhesion Molecule-1/biosynthesis*

OBJECTIVE: To measure the concentrations of soluble intercellular adhesion molecule-1 (s-ICAM-1), soluble vascular cell adhesion molecule-1 (s-VCAM-1), and von Willebrand factor (vWF) in the plasma of patients with rheumatic heart disease (RHD), and to provide basic theory for the mechanism of valvular and myocardial damage. METHODS: The consecutive patients with RHD (n=40) and healthy people (n=40) were chosen. All blood samples were taken from the peripheral veins. s-ICAM-1, s-VCAM-1 and vWF levels in all samples were measured by enzyme-linked immunosorbant assay. RESULTS: s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with RHD compared with healthy people (P < 0.01. The level of sICAM-1 was elevated in patients with atrial fibrillation compared with patients without atrial fibrillation. CONCLUSION The concentrations of s-ICAM-1, s-VCAM-1 and vWF levels were significantly elevated in patients with static rheumatic fever, which might be one of the pathogenic mechanisms of valvular damage, endothelial dysfunction, and myocardial damage in rheumatic heart disease.
Adult ; Atrial Fibrillation ; blood ; Female ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; Male ; Middle Aged ; Rheumatic Heart Disease ; blood ; Vascular Cell Adhesion Molecule-1 ; blood ; von Willebrand Factor ; metabolism

This study was aimed to investigate the expression of ICAM-1 (CD54) in pediatric tumor and acute leukemia (AL), so as to understand the distribution of ICAM-1 and its clinical significance. The expression of ICAM-1 in tissues of 46 pediatric tumor patients were detected by immunohistochemistry, and in bone marrow cells of 60 pediatric acute leukemia (AL) patients were detected by flow cytometry. 46 pediatric tumor patients included 10 lymphoma, 3 hepatoblastoma, 6 neuroblastoma, 2 rhabdomyosarcoma, 6 Ewing's bone sarcoma, 2 fibrosarcoma, 5 primitive neuroectodermal tumor, 11 nephroblastoma and 1 osteosarcoma. 60 AL pediatric patients included 20 acute lymphocytic leukemia (ALL) patients and 40 acute nonlymphocytic leukemia (ANLL) patients containing 20 M1, M2, M3 patients and 20 M4, M5. The results indicated that expression of ICAM-1 was more positive in all 3 hepatoblastoma cases, which represent a higher positive rate than that in lymphoma, neuroblastoma, rhabdomyosarcoma, Ewing's sarcoma of bone and osteosarcoma. However, no expression of ICAM-1 was observed in fibrosarcoma, nephroblastoma and primitive neuroectodermal tumor patients. On the other hand, the expression rate of ICAM-1 was 55 in ALL, 65 in ANLL M1, M2, M3, and 50 in ANLL M4, M5. It is concluded that the expression of ICAM-1 in pediatric tumor and AL has variability. The ICAM-1 positive expression is observed in hepatoblastoma and ANLL M1, M2, M3 patients, whereas it is undetectable in fibrosarcoma, nephroblastoma and primitive neuroectodermal tumor patients.
Child ; Cytokine-Induced Killer Cells ; Humans ; Immunotherapy ; Intercellular Adhesion Molecule-1 ; metabolism ; Leukemia ; metabolism ; therapy ; Neoplasms ; metabolism ; therapy

AIMTo observe the change of cardiovascular endothelium's ultrastructure and its intercellular adhesion molecules-1 (ICAM-1) expression in rat after repetitive high positive acceleration (+ Gz) exposures and further to explore the mechanisms of myocardial injuries induced by high + Gz stress.

METHODSThirty male Wistar rats were randomly divided into three groups: control group, + 1Gz group and + 10Gz group (n = 10 for each). The rats of + 10Gz group were exposed to five plateaus at + 10Gz for 30s with + 1Gz 1 min intervals, 3 times a week, for 3 weeks, while rats of + 1Gz group subjected to + 1Gz for 5 mim daily. The control group didn't undergo acceleration stress. The rats were decapitated in the next day after the last centrifuge run and myocardium were immediately dissected from left ventricles for ultrastructural examination using transmission electron microscope and immunohistochemical staining of ICAM-1.

RESULTSThe ultrastructural changes of the cardiovascular endothelium were observed in rats of 10Gz group, including endothelium edema and platelet aggregating in lumen of blood vessel. Also, the expression of ICAM-1 in + 10Gz stressed rats increased significantly (P < 0.05). While there was no difference between control group and + 1Gz group in ultrastructure of cardiovascular endothelium and its ICAM-1 expression.

CONCLUSIONThe results suggested that repeated high + Gz exposures could injury cardiovascular endothelium of rat and increase ICAM-1 expression, which indicated cell adhesion molecules (CAMs) inducing inflammation took part in myocardial injuries induced by high + Gz stress.

Acceleration ; Animals ; Endothelium, Vascular ; metabolism ; ultrastructure ; Intercellular Adhesion Molecule-1 ; metabolism ; Male ; Myocardium ; metabolism ; ultrastructure ; Rats ; Rats, Wistar

AIMTo investigate the role of ICAM-1 on the surface of vascular endothelial cell (VEC) in freezing/thawing injury of VEC, in order to elucidate the pathogenesis of freezing/thawing injury.

METHODSVEC separated and cultured from rat aorta and PMN separated from rat peripheral blood were selected as experiment materials. The frozen/thawed VEC model was founded by freezing VEC with the type WKL-V rate cooling instrument and then rewarming them in a water bath. ICAM-1 expression on the surface of frozen/thawed VEC was detected at 4, 12 and 24 h after freezing/thawing with immunohistochemical method. After coincubating frozen/thawed VEC with normal PMN, the adhesion of VEC to PMN was monitored with rose bengal staining assay and the injury level of VEC was indicated by measuring LDH activity in nutrient solution.

RESULTSThe ICAM-1 expression on the surface of VEC increased from 13.2% +/- 3.6% before freezing/thawing of VEC to 22.3% +/- 4.4% at 4 hour after freezing/thawing, and reached the peak (37.9% +/- 2.5%) at 12 hour after freezing/thawing of VEC. After coincubation of frozen/thawed VEC with normal PMN, the adherence of frozen/thawed VEC to PMN increased from group control 0.204 +/- 0.025 to 0.363 +/- 0.022 (P < 0.01), LDH activity in nutrient solution increased from group control 104.64 +/- 20.14 U/L to 162.33 +/- 27.88 U/L (P < 0.01), monoclonal antibody against ICAM-1 (ICAM-1 Mab) could partially block the adherence of frozen/thawed VEC to PMN (0.270 +/- 0.021, P < 0.01), and diminish LDH activity in nutrient solution (125.39 +/- 22.26 U/L, P < 0.05).

CONCLUSIONThe freezing/thawing of VEC can elicit an increase in ICAM-1 expression on the surface of VEC, and then proceed to VEC-PMN adherence and lead to VEC injury.

Animals ; Cells, Cultured ; Endothelial Cells ; metabolism ; Endothelium, Vascular ; cytology ; Freezing ; Intercellular Adhesion Molecule-1 ; metabolism ; Neutrophils ; cytology ; Rats

OBJECTIVETo study the effect of different CO2 pneumoperitoneum pressures on the expression of adhesion molecules of human gastric cancer cell line MNK-45.

METHODSMKN-45 cells in the experimental groups were exposed to simulated CO2 environment maintained at different pressures (1.2, 1.6, 2.0 kPa) for 4 hours. Control groups were exposed to room air. At the 0, 24, 48, 72, 96 hours after treatment, CD44v6, ICAM-1 and E-cadherin were detected by flow cytometry method.

RESULTSCD44v6 and ICAM-1 expressions showed pattern of firstly elevating, then descending to normal under the pressures of 1.2 kPa and 1.6 kPa. The expressions were different from control group significantly at 24 and 48 hours (P<0.01), while the 72 hours expression showed no difference compared with the controls (P>0.05). E-cadherin expression decreased significantly right after treatment compared to the control (P<0.01), but recovered to the level of control at 48 hours (P>0.05). In the 2.0 kPa group the expression changes of CD44v6, ICAM-1 and E-cadherin were more remarkable. CD44v6 and ICAM-1 expressions were increased significantly compared to control right after treatment (P<0.05). E-cadherin expression was significantly decreased even at 48 hours compared to the controls (P<0.01).

CONCLUSIONIn vitro CO2 pneumoperitoneum pressures have transient influence on the adhesion molecules expression of gastric cancer cell MKN-45, then those expressions can recover in a short-time.

Cadherins ; metabolism ; Carbon Dioxide ; Cell Adhesion Molecules ; metabolism ; Cell Line, Tumor ; Humans ; Hyaluronan Receptors ; metabolism ; Intercellular Adhesion Molecule-1 ; metabolism ; Pneumoperitoneum, Artificial ; Pressure ; Stomach Neoplasms ; metabolism

OBJECTIVE: Growth-arrest-specific protein 6 (Gas6) is a vitamin K-dependent protein and involved in cell proliferation, survival, adhesion and migration . Also it has been shown to play an important role in the inflammatory response .The aim of present study was to investigate the role of Gas6 in the process of the expression of adhesion molecules and chemokines of human umbilical vein endothelial cells (HUVECs) induced by Porphyromonas gingivalis lipopolysaccharide(P.g-LPS). METHODS: After up-regulation and down-regulation of the expression of Gas6, the vascular endothelial cells were stimulated with 1 mg/L P.g-LPS for 3 h and 24 h. Real-time quantitative polymerase chain reaction(real-time PCR) was taken to detect the expression of the cell adhesion molecules:intercellular adhesion molecule-1 (ICAM-1) and E-selectin, as well as chemokines:interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1). Wound healing assay was taken to observe the migration ability of endothelium cells in different groups. RESULTS: After 3 h of P.g-LPS stimulation, the expression of adhesion molecules and chemokine in the down-regulation group was not significantly different from that in the control group,while in the up-regulation group the decrease of E-selectin, ICAM-1, IL-8 and MCP-1 was 81%±0%, 47%±3%, 76% ± 3%, 26% ± 6% respectively. After 24 h of P.g-LPS stimulation, the expression of adhesion molecules and chemokine in down-regulation group was significantly higher than that in control group (2.06±0.07, 1.99±0.11, 3.14±0.15, 1.84±0.03 flod), while these molecules in the down-regulation group was significantly lower than in the control group (29%±1%, 62%±3%, 69%±1%, 41%±2%). Differences were statistically significant (P<0.01). Wounding healing assay showed that down-regulation of Gas6 enhanced migration ability of endothelial cells while up-regulation of Gas6 weakened this ability,which was consistent with the trend of real-time PCR result. CONCLUSION Down-regulation of the Gas6 gene enhanced the expression of ICAM-1, E-selectin, IL-8 and MCP-1 in HUVECs after P.g- LPS stimulating, while up-regulaiton of the Gas6 gene weakened the expression of ICAM-1, E-selectin, IL-8 and MCP-1 in HUVECs after P.g-LPS stimulating,suggesting that Gas6 may play a role in the process of endothelial cell adhesion.
Cell Adhesion ; Cell Adhesion Molecule-1 ; Cells, Cultured ; Chemokines/metabolism* ; E-Selectin/metabolism* ; Endothelium, Vascular ; Humans ; Intercellular Signaling Peptides and Proteins/physiology* ; Lipopolysaccharides ; Porphyromonas gingivalis/metabolism* ; Vascular Cell Adhesion Molecule-1/metabolism* ; Vitamin K

This study was purpose to compare and analyze the chronic lymphocytic leukemia human bone marrow stromal cells (CLL-hBMSC) and normal hBMSC (N-hBMSC) so as to provide theoretical evidence for establishment of CLL-hBMSC interaction model to imitate CLL microenvironment. Mononuclear cells (MNC) were isolated from bone marrow of CLL patients and healthy donors and then were cultured, hBMSC were established by expanding for at least five passages. The mRNA expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1), was analyzed by real-time PCR. The mRNA and protein expression of lymphotoxin beta receptor (LTβR) were determined by real-time PCR and Western blot, respectively. The individual NF-κB members at protein level of CLL-hBMSC and N-hBMSC were examined by Western blot. The effect of LTα1β2 on individual NF-κB family members at protein level in CLL-hBMSC and N-hBMSC was also examined by Western blot. The death of CLL cells was determined by flow cytometry with PI staining when cultured with or without CLL-hBMSC and N-hBMSC at different time points. The results showed that the hBMSC could be established successfully from bone marrow of CLL patients, which were similar to N-hBMSC. Adhesion molecules, such as VCAM-1 and ICAM-1, were found to be expressed at similar mRNA levels in CLL-hBMSC and N-hBMSC. LTβR expressions at mRNA and protein levels were comparable between CLL-hBMSC and N-hBMSC. The protein expression of the individual NF-κB family members could be detected in CLL-hBMSC and N-hBMSC with similar expression levels. LTα1β2 stimulation activated both the classical ( RelA/p50 ) and alternative ( RelB/p52 ) NF-κB complexes in CLL-hBMSC and N-hBMSC. The capacities of CLL-hBMSC and N-hBMSC to protect CLL cell survival were similar. It is concluded that there is no statistical difference between bone marrow from healthy donors and CLL patients in the efficiency of generating of hBMSC. LTβR-NF-κB signaling molecules are expressed and activated on hBMSC with a similar pattern.
Humans ; Intercellular Adhesion Molecule-1 ; metabolism ; Leukemia, Lymphocytic, Chronic, B-Cell ; genetics ; metabolism ; pathology ; Lymphotoxin beta Receptor ; metabolism ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Signal Transduction ; Transcription Factor RelA ; metabolism ; Transcription Factor RelB ; metabolism ; Vascular Cell Adhesion Molecule-1 ; metabolism

OBJECTIVETo explore the role of intercellular adhesion molecule-1 (ICAM-1) and regulated upon activation normal T cell expressed and secreted (RANTES) in bronchiolitis and their correlation in the pathogenesis of this disorder.

METHODSThe expression of ICAM-1 was detected by flow cytometry on lymphocytes of peripheral blood in 28 infants with bronchiolitis, 23 infants with bronchopneumonia and 24 healthy infants. Serum level of RANTES was assayed using ELISA. The correlation between ICAM-1 and RANTES levels was evaluated using Pearson correlation coefficient.

RESULTSThe ICAM-1 level in the bronchiolitis group (35.0+/-10.3%) was much higher than that in the bronchopneumonia (29.9+/-8.6%; p<0.05) and the control groups (24.6+/-6.9%; p<0.01). The bronchopneumonia group had higher ICAM-1 level than the control group (p<0.05). The RANTES level in the bronchiolitis (32.1+/-6.0 ng/mL) and the bronchopneumonia groups (30.6+/-6.2 ng/mL) was significantly higher than that in the control group (27.1+/-5.1 ng/mL) (p<0.01, p<0.05, respectively), however, no significant difference was found between the bronchopneumonia and bronchiolitis groups. There was a positive correlation between ICAM-1 and RANTES levels in the bronchiolitis group (r=0.675, P<0.01).

CONCLUSIONSICAM-1 and RANTES are involved in the pathogenesis of bronchiolitis and show a synergistic effect.

Bronchiolitis ; etiology ; metabolism ; Chemokine CCL5 ; analysis ; physiology ; Child, Preschool ; Female ; Humans ; Infant ; Intercellular Adhesion Molecule-1 ; analysis ; physiology ; Male

Mechanical environment seems to be one of the most important surviving environment for vessel conduit and vascular endothelial cells(ECs), while adhesion is one of the most important physical characteristics of ECs. In this study, Flow chambers of steady laminar and turbulent flow are made and improved. Different flow-derived VCAM-1, ICAM-1 expressions are detected by laser confocal microscope. Spacial and temporal curves of the adhesion molecules are protracted. In laminar flow, expression of VCAM-1 is dramatically elevated, whereas the expression of ICAM-1 is transiently elevated and it immediately falls back to the baseline. In turbulent flow, expression of VCAM-1 declines, while expression of ICAM-1 slowly rises to a peak. These results indicate that such pathological flow field as turbulence exerts different influence on the adhesion of vascular ECs from laminar flow, and turbulence could be one of the most important reasons of the ECs structural and functional lesion.
Cell Adhesion ; Cells, Cultured ; Endothelium, Vascular ; cytology ; metabolism ; Epithelial Cells ; cytology ; metabolism ; Humans ; Intercellular Adhesion Molecule-1 ; biosynthesis ; Microscopy, Confocal ; Stress, Mechanical ; Umbilical Veins ; cytology ; Vascular Cell Adhesion Molecule-1 ; biosynthesis