OBJECTIVETo explore the protein expression of heme oxygenase-1 (HO-1) and platelet endothelial cell adhesion molecules-1 (PECAM-1) in human coronary artery endothelial cells induced with Zinc Oxide Nanoparticle (ZnO-NPs).

METHODSMTT assay was used to determine the cell viability of ZnO-NPs. Levels of HO-1 and PECAM-1 protein in culture supernatants were measured using ELISA after human coronary artery endothelial cells were treated with different concentrations (0, 10, 20, 40µg/ml) of ZnO-NPs for 24 h.

RESULTSThe cell viability of human coronary artery endothelial cells in each group was 89.76%, 83.61%, 63.10%, 53.20%, 48.11%, 42.35%, 38.06%, 25.44% respectively when treated with different concentrations of ZnO-NPs (12.5, 25, 50, 70, 80, 90, 100, 200µg/ml). Protein levels of HO-1 (ng/L) in each group were 0.041±0.011, 0.512±0.076, 0.906±0.059, 1.062±0.089 respectively after the stimulation of different concentrations of ZnO-NPs (0, 10, 20, 40µg/ml). Comparisons in each group were statistically significant (P < 0.05). Protein levels of PECAM-1 (µg/L) in each group were 7.966 ± 0.046, 7.993 ± 0.036, 8.629 ± 0.052, 8.811 ± 0.039 respectively after the stimulation of different concentrations of ZnO-NPs (0, 10, 20, 40 µg/ml). Compared with the control group, protein levels of PECAM-1 increased (P < 0.05) when the concentration of ZnO-NPs was 20µg/ml or 40 µg/ml.

CONCLUSIONZnO-NPs stimulation could inhibit the viability of human coronary artery endothelial cells and upregulate the protein expression of HO-1 and PECAM-1.

Blood Platelets ; Cell Survival ; Coronary Vessels ; Endothelial Cells ; drug effects ; Heme Oxygenase-1 ; metabolism ; Humans ; Nanoparticles ; toxicity ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Zinc Oxide ; toxicity

The murine bone marrow endothelial cell line (mBMEC) has been maintained by means of subculture and cryopreservation for over 10 years since it was established in our laboratory. This study was aimed to newly identify biological characteristics of this cell line for further study. The cultured mBMEC cells were observed by inverted microscopy and transmission electron microscopy (TEM). PECAM-1 (CD31) and von Willebrand factor (vWF) were detected by immunofluorescent staining. The phagocytotic activity of the cells in culture was tested by using fluorescent acetylated low-density lipoprotein (Dil-Ac-LDL). The cell growth kinetics analysis and karyotype analysis were performed. The results showed that the adherent cells were mostly elliptical, rounded and spindle-shaped, and some of them connected to each other to form cord- and network-like arrangements in mBMEC cultures at subconfluence. The adherent cells grew up to confluence as a cobblestone-like monolayer. Several ultrastructural features of the endothelial cells could be observed in TEM sections of the cultured cells. More than 94% of mBMEC cells were positive for either CD31 or vWF. The phagocytotic ingestion of Dil-Ac-LDL occurred in 98.5% of cells. In normal culture conditions, the cells grew with a mean population doubling time of 54.6 hours and the maximal mitotic index was 38 per thousand in the rapid growth period. The colony yields were 4.33% to 7.40% depending on the plating density of cells. Karyotypes of all the cells were aneuploidy with a greater percentage of hyperdiploid. It is concluded that mBMEC cells retain the fundamental properties of endothelial cells, but the growth kinetics and biological behaviors are slightly different from those in the early days after the establishment of this cell line.
Animals ; Bone Marrow Cells ; cytology ; Cell Line ; Endothelial Cells ; cytology ; physiology ; Karyotyping ; Mice ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; von Willebrand Factor ; metabolism

Acute Disease ; Adolescent ; Adult ; Aged ; Biopsy, Needle ; Endothelial Cells ; metabolism ; Female ; Graft Rejection ; diagnosis ; Hepatocytes ; metabolism ; Humans ; Immunohistochemistry ; Intercellular Adhesion Molecule-1 ; metabolism ; Liver ; metabolism ; pathology ; Liver Transplantation ; Male ; Middle Aged ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Young Adult

OBJECTIVE: To explore the effect of Fuzheng Huayu (FZHY) recipe on the fenestration of capillarization in liver sinusoidal endothelial cells (LSECs).
 METHODS: Ten Sprague Dawley (SD) rats were fed with 0.46 g/kg FZHY powder by intragastric administration. Two hours later, a second gavage were given to the rats. The serum from rat heart at 1 hour after second gavage was collected (FZHY group, n=10). Another ten SD rats was administrated with distilled water through the same process and served as the control (control group, n=10). The serum from both groups were separately diluted with Dulbecco minimum essential medium (DMEM) for 10% and served as the culture medium for LSECs. At the different conditions, the vWF and CD31 expressions were detected by immunocytochemistry and Western blot, while the changes of LSECs fenestrae structure were observed under scanning electron microscopy.
 RESULTS: 1) Immunocytochemistry and Western blot showed that the vWF and CD31 protein levels were lower in LSECs in the FZHY group than those in the control group. The gray levels of vWF and CD31 protein were 0.548±0.020 and 0.262±0.010 in the FZHY group, and 0.845±0.090 and 0.383±0.010 in the control group respectively, with statistical significant difference (t=5.18, 9.61, both P<0.05). 2) The results from scanning electron microscopy showed that the fenestration of LSECs was closed and almost lost in the control group, but many fenestra appeared in the LSECs in the FZHY group.
 CONCLUSION FZHY recipe can suppress the expression of vWF and CD31, increase the fenestrae on the LSECs surface and reverse the capillarization of LSECs.
Animals ; Drugs, Chinese Herbal ; pharmacology ; Endothelial Cells ; cytology ; drug effects ; Liver ; cytology ; Platelet Endothelial Cell Adhesion Molecule-1 ; chemistry ; Rats ; Rats, Sprague-Dawley ; von Willebrand Factor ; chemistry

OBJECTIVETo investigate the distributions of genotypic and allelic frequencies of intercellular adhesion molecule-1 (ICAM-1) gene K469E and platelet endothelial cell adhesion molecule-1 (PECAM-1) gene C373G in patients with preeclampsia.

METHODSPolymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) and DNA sequencing were used for detecting ICAM-1 gene K469E and PECAM-1 gene C373G genotypes in 110 women with preeclampsia and 110 normotensive pregnant women in comparison with their clinical characteristics.

ESULTSThe distributions of observed and expected genotype frequencies were consistent with Hardy-Weinberg equilibrium. No significant differences were found in the genotype and allele frequencies of ICAM-1 gene K469E between the two groups (P>0.05), but the CC and the CG genotype frequencies of PECAM-1 gene C373G were significantly different between them (P<0.05). The relative risk for preeclampsia of CG genotype was 1.959 folds of that in CC genotype carriers (OR=1.959, 95%CI: 1.090-3.520, P=0.024), and this association still existed after adjustment for age, gravidity, parity and BMI in logistic regression models. The C373G allele frequencies showed no significant difference between the two groups (P>0.05).

CONCLUSIONSThe CG genotype of PECAM-1 gene C373G genetically predispose the carriers to preeclampsia, while ICAM-1gene K469E polymorphisms is not associated with preeclampsia.

Adult ; Case-Control Studies ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; Platelet Endothelial Cell Adhesion Molecule-1 ; genetics ; Polymorphism, Genetic ; Polymorphism, Restriction Fragment Length ; Pre-Eclampsia ; genetics ; Pregnancy ; Sequence Analysis, DNA

OBJECTIVETo observe the atherogenic lesion progress in a novel ischemia/reperfusion induced atherosclerosis model in the carotid artery of rats.

METHODSRats were divided into normal control, sham-operated control and ischemia-reperfusion injury (IRI) groups (n = 10 each). IRI was induced by 30 min carotid artery occlusion with a 2 cm long artery clips in anesthetized rats. Four weeks later, hematoxylin and eosin (HE) and immunohistochemical stain were performed on carotid arteries of various groups. The ratio of neointima area/media area (I/M) and expression of platelet endothelial cell adhesion molecule (PECAM-1/CD31) were compared among groups.

RESULTS(1) Neointimal hyperplasia was detected in carotid artery of IRI group and the I/M ratio was significantly higher than in normal control and sham-operated groups (1.328 ± 0.301 vs. 0.011 ± 0.004 and 0.017 ± 0.008, all P < 0.01). (2) Small to large-sized neointima were found in the IRI group and the small sized intima was stable while large sized intima which covered the whole cavity was instable and underwent spontaneous rupture and thrombosis formation. (3) CD31 expression was significantly upregulated in carotid artery of IRI group corresponding to the instability of neointima in this group.

CONCLUSIONIschemia-reperfusion injury of carotid artery could result in atheroma in rats, this model could be used for future research on the pathogenesis of atherosclerosis. Our results show that endothelium injury of the arteries is the key factor to trigger atheroma and responsible for the disruption of the plaque.

Animals ; Carotid Artery, Common ; pathology ; Disease Models, Animal ; Endothelium, Vascular ; pathology ; Male ; Plaque, Atherosclerotic ; pathology ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury

OBJECTIVESTo study the expression of CD34, CD31, CD14, CD10 and factor VIII on blood island of yolk sac (YS), PAS/aorta-germen-mesonephros (AGM) region and hepatic hematopoietic foci.

METHODSThirty-two cases of 3rd-12th weeks human embryo were obtained by drug abortion. Paraffin embedded sections with H.E staining and immunohistochemistry reaction (SABC) were performed.

RESULTSYS blood island of 3rd-4th weeks of gestation was consisted of two types of cells. One was vascular endothelial cells located outside and the other hematopoietic cells inside the blood island. Both the two types of cells were CD10, CD14, CD31 and factor VIII positive. Hematopoietic cells were CD34 negative, and vascular endothelial cells were CD34 positive. On 32nd days of gestation, the hematopoietic cells migrated out of YS. On 4th week of gestation, CD34, CD14, CD10, CD31 and factor VIII positive cells appeared in the aorta, mesonephros and hepatic hematopoietic foci. By the 7th week, the number of positive hematopoietic cells reached the peak. In 11th-12th weeks, most cells in these regions were matured red blood cells and were negative for all the antibodies mentioned above excepting for CD34. During 4th-12th weeks, all endothelial cells in embryo were CD34 positive.

CONCLUSIONSThe hematopoietic cells and endothelial cells of YS blood island co-expressed CD10, CD14, CD31 and factor VIII. Endothelial cells were CD34 positive but hematopoietic cells were negative in YS blood island. The hematopoietic cells of aorta, mesonephros and hepatic hematopoietic foci expressed CD34, CD10, CD14 and factor VIII from 4th week to 7th week. Anti-CD34 antibody could label endothelial cells of every kinds vessels of embryo from 3rd to 12th weeks.

Antigens, CD34 ; metabolism ; Factor VIII ; metabolism ; Fetus ; metabolism ; Humans ; In Vitro Techniques ; Lipopolysaccharide Receptors ; metabolism ; Liver ; metabolism ; Neprilysin ; metabolism ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Yolk Sac ; metabolism

OBJECTIVETo investigate the role of expression of platelet membrane glycoprotein CD31, CD61 and CD62p in the pathogenesis of decompression sickness.

METHODSMice were randomly divided into decompression sickness group and normal control group. The animals in decompression sickness group were exposed to 600 kPa compressed air for 60 minute, then they were rapidly decompressed to normal pressure in one minute. At 60th minute after reducing to normal pressure, the expression of CD31, CD61 and CD62p on platelet membrane in mice was measured by flow cytometry.

RESULTSThe mean fluorescence intensity of CD31, CD61 and positive percentage of CD62p on platelet membrane [(18.64 +/- 1.01), (271.06 +/- 24.25), (4.48% +/- 0.43%) respectively] in decompression sickness group were significantly increased compared with normal control group [(16.89 +/- 1.69), (234.09 +/- 15.96), (3.00% +/- 0.66%) respectively] (P < 0.05, P < 0.01).

CONCLUSIONInadequately rapid decompression may induce up regulation of platelet membrane glycoprotein CD31, CD61 and CD62p expression in mice, which may lead to thrombosis.

Animals ; Blood Platelets ; chemistry ; Decompression Sickness ; blood ; Female ; Integrin beta3 ; blood ; Mice ; P-Selectin ; blood ; Platelet Endothelial Cell Adhesion Molecule-1 ; blood

BACKGROUNDThe clinical applications of fibrin glue span over several surgical modalities. The aim of this study was to evaluate the biocompatibility and biodegradation of different formulations of platelet-rich fibrin glue in vivo and examine its effects on the neovascularization of wound sites.

METHODSHuman-derived single-unit fibrin glue was prepared. Incisions were made on the backs of rats, and these were coated with homemade glues containing different concentrations of aminomethylbenzoic acid (Groups A-F) or commercial adhesives (Group G). A sham control group was included (Group H). The wounds were examined by histological analysis and immunohistochemistry at several time points.

RESULTSSuccessful wound closure was achieved in all groups by day 12. Acute inflammation occurred during the first six days, but gradually disappeared. The longest sealant duration was achieved using the lowest concentration of anti-fibrinolytic agent in a 1:10 volume ratio with cryoprecipitate. Expression levels of the platelet endothelial cell adhesion molecule-1 were significantly higher in Groups A and C compared to the control groups (Groups G and H) on day 3 (P < 0.05).

CONCLUSIONSSingle-unit platelet-rich fibrin glue has excellent biocompatibility and is associated with the upregulation of neovascularization. The addition of aminomethylbenzoic acid could prevent the degradation of fibrin glue.

Animals ; Female ; Fibrin Tissue Adhesive ; adverse effects ; therapeutic use ; Humans ; Immunohistochemistry ; Platelet Endothelial Cell Adhesion Molecule-1 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Wound Healing ; drug effects

Aged ; Antigens, CD34 ; Humans ; Immunohistochemistry ; Lymphangioma ; diagnosis ; etiology ; pathology ; Male ; Orthopedic Procedures ; adverse effects ; Platelet Endothelial Cell Adhesion Molecule-1 ; Postoperative Complications ; Skin Neoplasms ; diagnosis ; etiology ; pathology