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Objective To investigate the relationship between platelet endothelial cell adhesion molecule I (PEC AMI )/leiomodin 1 ( LMOD1 ) gene polymorphism loci and the risk of carotid plaque vulnerability in patients with ischemic stroke. Methods Ischemic stroke patients with carotid plaque admitted to Beijing Tiantan Hospital from May 2014 to October 2017 were enrolled prospectively. The demographic data and relevant clinical information were collected Carotid artery high-resolution magnetic resonance imaging (MRI) was used to distinguish vulnerable and stable plaques. The patients were enrolled in vulnerable plaque group and stable plaque group in turn. Real-time polymerase chain reaction was used. The TaqMan probe was use to conduct genotyping and statistical analysis of the PECAM1 ,LMOD1 gene polymorphism loci rsl 867624 and rs2820315 in the vulnerable plaque group and the stable plaque group. Binary logistic regression analysis was used to investigate the risk factors affecting the vulnerability of carotid atherosclerotic plaques. Results A total of 270 ischemic stroke patients with carotid plaque were enrolled, including 189 with vulnerable plaques and 81 with stable plaques. The polymorphism analysis of the PECAM1 gene locus rsl867624 in the two groups showed that the allele T was a vulnerable plaque risk gene,and its gene frequency in the vulnerable plaque group and the stable plaque group was 87. 3% (330/378) and 79. 6% (129/162;OR, 1.759,95% CI 1.080 -2.864 respectively,P = 0. 022). Analysis of the LM0D1 gene SNP locus rs2820315 showed that allele C was a risk gene for vulnerable plaques,and its gene frequency in the vulnerable plaque group and the stable plaque group was 87.6% (331/378) and 80.9% respectively (13I/I62;0tf, I. 667,95% CI 1. 014 -2. 738, P =0. 042). Logistic regression analysis showed that age (OR, 1.069,95% CI 1.022-1. 118, P = 0.004 ),PECAM1 gene rsl867624 locus T/T genotype (OR, 2.202,95% CI 1. 035 -4. 688 tP =0. 041) ,and LMODl gene rs2820315 locus C/C genotype ( OR,2. 199,95% CI 1. 005 -4. 809 , P =0.048) were the risk factors for the formation of vulnerable plaques. Conclusion The single nucleotide polymorphism locus rsl867624 of PECAM1 gene and single nucleotide polymorphism locus rs2820315 of LMODl gene were associated with carotid plaque vulnerability.
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Objective To investigate the expressions of soluble platelet endothelial cell adhesion molecule-1 (PECAM-1) and P-selectin and the clinical significance in autistic children.Methods Enzyme-linked immunosorbent assay (ELISA) was used to detect serum PECAM-1 and P-selectin levels in 12 autistic children and 15 healthy children,the autistic children were scored by using Antecedent Behavior Consequence (ABC) Chart,and correlation analysis of PECAM-1 and ABC Chart was performed.Results The PECAM-1 level in autistic children was higher than that in healthy control group(t =2.06,P ＜ 0.05),and the P-selectin level was lower than that in healthy control group (t =2.05,P ＜ 0.05),at the same time,PECAM-1 level was positively correlated with the ABC scores in autistic children (r =0.67,P =0.017).Conclusions PECAM-1 as a representation of the immune system immune factors may be involved in the central nervous immune process of autistic children,which is related to ABC chart scores of autistic children.Also it prompts that autism is related to immune factors.
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BACKGROUND: Platelet endothelial cell adhesion molecule-1 (PECAM-1), also known as CD31, is mainly distributed in vascular endothelial cells. Studies have shown that PECAM-1 is a very significant indicator of angiogenesis, and has been used as an indicator for vascular endothelial cells. The present study aimed to explore the relationship between the expression of PECAM-1 and the degree of acute lung injury (ALI) and fibrosis in paraquat (PQ) induced lung injury in rabbits. METHODS: Thirty-six adult New Zealand rabbits were randomly divided into three groups (12 rabbits in each group) according to PQ dosage: 8 mg/kg (group A), 16 mg/kg (group B), and 32 mg/kg (group C). After PQ infusion, the rabbits were monitored for 7 days and then euthanized. The lungs were removed for histological evaluation. Masson staining was used to determine the degree of lung fibrosis (LF), and semi-quantitative immune-histochemistry analysis to determine the expression of PECAM-1. Pearson's product-moment correlation analysis was performed to evaluate the relationship between the expression of PECAM-1 and the extent of lung injuries expressed by ALI score and degree of LF. RESULTS: Rabbits in the three groups showed apparent poisoning. The rabbits survived longer in group A than in groups B and C (6.47±0.99 days vs. 6.09±1.04 days vs. 4.77±2.04 days) (P<0.05). ALI score was lower in group A than in groups B and C (8.33±1.03 vs. 9.83±1.17 vs. 11.50±1.38) (P<0.05), and there was statistically significant difference between group B and group C (P=0.03). LF was slighter in group A than in groups B and C (31.09％±2.05 ％ vs. 34.37％±1.62％ vs. 36.54％±0.44％) (P<0.05), and there was statistically significant difference between group B and group C (P=0.026). The PEACAM-1 expression was higher in group A than in groups B and C (20.31％±0.70％ vs. 19.34％±0.68％ vs. 18.37％±0.46％) (P<0.05), and there was statistically significant difference between group B and group C (P=0.017). Pearson's correlation analysis showed that the expression of PECAM-1 was negatively correlated to both ALI score (Coe=–0.732, P=0.001) and degree of LF (Coe=–0.779, P<0.001). CONCLUSIONS: The PECAM-1 expression significantly decreases in New Zealand rabbits after PQ poisoning, and the decrease is dose-dependent. The PECAM-1 expression is negatively correlated with ALI score and LF, showing a significant role in the development of lung injuries induced by PQ.
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Background To study diabetic retinopathy (DR) related risk factors is very important in the prevention of DR.Platelet endothelial cell adhesion molecule-1 (PECAM-1) is an important mediator that mediates high blood glucose-induced vascular diseases in diabetic patients.However,its mechanism is still below understood.Objective This clinical study was to investigate the effect of serum level changes of PECAM-1 on DR in type 2 diabetic patients.Methods Fifty-four patients with type 2 diabetes were enrolled from the endocrinology department of the Third People' s Hospital of Nantong City.Fundus examination was performed using the ophthalmoscope and fundus fluorescence angiography (FFA) on all the patients,and these patients were grouped as the non-DR (NDR)group (18 cases),non-proliferative DR(NPDR) group (20 cases) and proliferative DR group (PDR) (16 cases) based on the DR staging criterion of the Chinese Medical Association (1987 version).Eighteen age-and gender-matched normal subjects served as the normal control group.Peripheral blood was collected,and serum PECAM-1 levels were assayed using ELISA.Serum HbA1c levels were detected using the high performance liquid colorimetric(HPLC) method.The correlation of serum PECAM-1 level with serum HbA1c level was analyzed.All results were compared among the groups.Results The serum PECAM-1 levels were (10.907 ± 2.792),(7.024 ±2.377),(5.231 ± 1.816) and (3.817 ± 1.045) μg/L,respectively,in the PDR group,NPDR group,NDR group and normal control group,showing a significant difference among the 4 groups (F =12.630,P =0.02).Serum PECAM-1 content was significantly higher in the PDR group when compared with the NPDR group,NDR group and normal control group (P＜0.05).The serum HbA1c levels were (12.596±3.148)％,(9.118±3.356)％,(5.491±1.017)％ and (4.992 ± 0.725)％ in the PDR group,NPDR group,NDR group and normal control group,respectively,with a significant difference among these 4 groups (F =7.130,P =0.015),and those in the PDR group and NPDR group were significantly elevated in comparison with the NDR group and normal control group (P＜0.05).Significantly positive correlations were seen between serum PECAM-1 level and HbA1 c level in the PDR group,NPDR group and NDR group (r=0.799,P＜0.01 ;r =0.647,P＜0.01 ;r =0.685,P＜0.01).Significantly more patients with a disease course of ≥ 10 years were in the NPDR group in comparison with the PDR group (P =0.023).Conclusions Increase of serum PECAM-1 level is closely associated with blood glucose level,and it is an important factor in the pathogenesis and development of DR.These results imply that control of blood glucose is crucial for the prevention of DR in patient with type 2 diabetes.
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Stress has long been known to be a causative factor of various disease states. In this study, we investigated the effects of repeated restraint stress on platelet endothelial cell adhesion molecule-1 (PECAM-1), a very important mediator in inflammation, immunoreactivity and protein levels as well as neuronal damage, in the gerbil hippocampus after 5 minutes of transient cerebral ischemia. Transient ischemia-induced neuronal death was shown in CA1 pyramidal cells 4 days after ischemia/reperfusion. However, repeated restraint stress protected neuronal death induced by ischemic damage. In the ischemia-group, PECAM-1 immunoreactivity and its protein levels were significantly increased in all the hippocampal subregions 4 days after ischemia/reperfusion. However, PECAM-1 immunoreactivity and its protein levels did not change significantly in the hippocampus of the stress-ischemia-group compared to the sham-groups. These results indicate that repeated restraint stress protects neuronal damage induced by transient cerebral ischemia, and this may be associated with maintenance of PECAM-1levels.