Objective To study the change in serum levels of soluble CD14, tumor necrosis factor-α, E-selectin, interleukin-10 and mean arterial pressure, as well as their relationship to infection during the pathophysiologic process in endotoxemia of rabbits. Methods Sixteen rabbits were randomly divided into two groups: group A, as a control group; group B, endotoxemia group. The model of rabbit with endotoxemia were used. Endotoxin at a dose of 1.5 mg/(kg·h) or 3 mg/(kg·h) was continuously infused through external jugular vein within 2 hours, 1 hour respectively. The change of levels of serum soluble CD14, tumor necrosis factor-α, interleukin-10 and E-selectin were observed at 0 (time before infusion of endotoxin), 30, 60, 120, 180, 240, 300 minutes, while mean arterial pressure was measured by polygraphy system. Results In the group B,there was an increase of content of soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin following 30, 120 minutes respectively,and mean arterial pressure was lower than that of group A at same time points. Conclusion The results suggest that soluble CD14,tumor necrosis factor-α,interleukin-10 and E-selectin may play an important role during the change of infection and that these changes may be closely related with severe infection.
Objective To compare the in vitro inhibition activity of three mimic peptides at lipopolysaccharide binding protein (LBP)／CD14 binding sites for LPS-induced inflammatory response.Methods Enzyme-linked immunoSorbent assay(ELISA)was applied for the detection of the affinity between the mimic peptides and CD14 as well as the competitive inhibition activity of LBP.Mature U937 cells induced by PMA were co-cultured with LPS and intervened by mimic peptide.The effect of the mimic peptide on the TNF-α expression of U937 was detected by RT-PCR.Alveolar macrophages(AMs)of rats were co-cultured with FITC-LPS，and mimic peptide intervention was conducted.The effect of the mimic peptide on combination of LPS and AMs was observed by fluorescence microscope . Results Affinity between No.1 mimic peptide(FHRWPTWPLPSP，10 μg／mL)and CD14 was significantly higher than those of No.2 and No.3(20.3±4.1 11.8±2.4 and 13.7±3.3，Plt;0.01 or Plt;0.05).The competitive inhibitory activity of No.1 mimic peptide(10 μg／mL)for LBP was higher than those of No.2 and No.3[(57.2土11.2)％ vs(39.4±9.7)％ and(37.9±8.3)％ ，Plt;0.01].All of the three mimic peptides(10 μg／mL)could significantly inhibit the LPS-induced expression of TNF-α by U937 at mRNA level(Plt;0.01 or Plt;0.05)，moreover，the inhibitory activity of No.1 peptide was the highest(0.239±0.053 vs 0.406±0.112 and 0.493±0.121，Plt;0.01).In addition，No.1 mimic peptide markedly inhibited LPS combination with rat lung AMs(2157±514 vs 2763±453，plt;0.01).Conclusion No.1 mimic peptide(FHRWPTWPLPSP)have a relatively higher affinity with CD14 and high competitive inhibition activity for LBP，therefore it have the potential ability of anti-inflammatory response induced by LPS.
ObjectiveTo summary the relationship between CD147 and the occurrence and development of hepatocellular carcinoma, and its roles in clinical diagnosis and treatment. MethodReferring to the related literatures in recent years at home and abroad, the concept of CD147, and its relationship with the occurrence, development, invasion, and metastasis of hepatocellular carcinoma were reviewed. ResultsCD147 plays a key role in the development, progress, invasion, and metastasis of hepatocellular carcinoma. CD147 can be used as a long-term outcome predictor for hepatocellular carcinoma patients and also began to show its in hepatocellular carcinoma target therapy. ConclusionThere are numerous studies about the relationship between CD147 and hepatocellular carcinoma, but still exists some problems to be further studied.
ObjectiveTo observe the expression of CD147, matrix metalloproteinases-2 (MMP-2) and vascular endothelial growth factor (VEGF) in a rat model of oxygen induced retinopathy (OIR). MethodsEighty-four neonatal Wistar rats were divided into two groups randomly, the hyperoxia group (n=42) and the control group (n=42). Oxygen induced retinopathy was established in the hyperoxia group, the control group was raised in room air. Wholemonts were prepared from postnatal day (p) 7 and 14 rat retina to observe retinal vascular morphology. The number of endothelial cells to break through the internal limiting membrane was counted from p14 retinal paraffin sections. Expression of CD147, MMP-2 and VEGF protein levels was analyzed by immunohistochemistry on p12, p14, and p16 retinal sections. At the meantime, correlation between CD147 and MMP-2, VEGF was analyzed by two-way analysis of variance (ANOVA) test. ResultsAt p7, the retinal vasculature of the control group was radial distributed with large caliber. In OIR group, there were vasoconstriction, large area of avascular zone and a few small areas of vascular network. At p14, the normal untreated rat had interwoven retinal vasculature, but in OIR group, the retinal vasculature was expanded and tortuous, and forming lots of neovascular cluster in the boundary of the perfusion and non-perfusion regions resulting exudation and hemorrhage. At p14, the endothelial cell nuclei breakthrough the internal limiting membrane was (1.30±1.26) and (19.70±3.56) respectively in control and OIR group, the difference was statistically significant (t=21.813, P<0.01). Immunohistochemical staining showed that CD147, MMP-2, VEGF expression was low in control group but high in OIR group. From p12 to p16, CD147, MMP-2 and VEGF protein expression increased in OIR retinas compared with control samples(p12:t=5.612, 4.122, 4.955; P<0.01. p14:t=11.390, 8.047, 12.176; P<0.01. p16:t=6.355, 4.422, 5.110; P<0.01). ConclusionCD147, MMP-2 and VEGF were highly expressed in the rat model of oxygen induced retinopathy.
ObjectiveTo investigate the value of serum soluble CD146 (sCD146) in determining acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) resistance in lung adenocarcinoma.MethodsA total of 144 lung adenocarcinoma EGFR sensitive patients in People’s Hospital of Zhengzhou University diagnosed from January 2016 to December 2016 were recruited in the study. According to the different time of taking drugs, the patients were divided into a non-medication group (31 cases), a 1 to 3 month treatment group (25 cases), a 4 to 6 month treatment group (19 cases), a 7 to 12 month treatment group (25 cases), a drug-resistant group (24 cases), and a nonresistant group up to 1 year of treatment (20 cases). The serum levels of sCD146, carcinoembryonic antigen (CEA) and neuron-specific enolase (NSE) were measured by ELISA and chemiluminescence and compared between different period of medication. The relationship of serum sCD146 with tumor markers (CEA, NSE) and tumor related clinical parameters (age, gender, tumor stage, metastasis, tumor diameter, number of the lesions) were analyzed.ResultsThe serum sCD146 level was minimum in the non-medication group that did not receive pioglitazone treatment, highest in the 1 to 3 month treatment group (early treatment period), and declined with duration of medication until resistance occurred without significant difference (P>0.05). The level of sCD146 of the drug-resistant group was significantly lower than that of all nonresistant groups, with significant difference (allP<0.05), but still higher than that of the non-medication group (P<0.05). The serum sCD146 levels in the nonresistant patients with medication over 1 year and within 1 year were similar (P>0.05), and significantly higher than the non-medication group and drug-resistance group (allP<0.05). The serum CEA levels did not differ significantly between 6 groups (P>0.05). The serum NSE level of the 4 to 6 month treatment group was lower than that of the 7 to 12 month treatment group (P<0.05), but both in the normal reference range. The NSE levels did not differ in any other groups (P>0.05). Serum sCD146 was associated with metastasis (P<0.05), but not associated with serum CEA or NSE, nor with sex, age, tumor staging, tumor diameter or lesion number (allP>0.05).ConclusionsCD146 may be involved in the mechanism of TKI killing tumor cells and the mechanism of TKI resistance, and may be a serological marker for monitoring the efficacy of TKI and judging the resistance of TKI.
ObjectiveTo summarize the expression and role of CD146 in mesenchymal stem cells (MSCs).MethodsThe literature related to CD146 at home and abroad were extensively consulted, and the CD146 expression in MSCs and its function were summarized and analyzed.ResultsCD146 is a transmembrane protein that mediates the adhesion of cells to cells and extracellular matrix, and is expressed on the surface of various MSCs. More and more studies have shown that CD146+ MSCs have superior cell properties such as greater proliferation, differentiation, migration, and immune regulation abilities than CD146- or unsorted MSCs, and the application of CD146+ MSCs in the treatment of specific diseases has also achieved better results. CD146 is also involved in mediating a variety of cellular signaling pathways, but whether it plays the same role in MSCs remains to be demonstrated by further experiments.ConclusionThe utilization of CD146+ MSCs for tissue regeneration will be conducive to improving the therapeutic effect of MSCs.
ObjectiveTo summarize the mechanism of CD147 in breast cancer invasion and metastasis, treatment, and drug resistance so as to provide reference for clinical decision-making.MethodThe relevant literatures about studies of CD147 in breast cancer in recent years were reviewed.ResultsCD147 was widely distributed in vivo and highly expressed in malignant tumor tissues. CD147 promoted matrix metalloproteinases and vascular endothelial growth factor productions and tumor microenvironment generation by extracellular matrix in breast cancer through different mechanisms. It degraded extracellular matrix and stimulated neovascularization to promote tumor invasion and metastasis. Related studies had shown that CD147 was highly expressed in the breast cancer tissues and which was associated with tumor grade and prognosis in patients with breast cancer, and it was a biological marker for diagnosis of breast cancer. However, a large of drugs targeted for CD147 and its involved pathways didn’t well benefit patient with breast cancer due to the failure of clinical trials and chemotherapy resistance.ConclusionsCD147 plays a key role in development, invasion and metastasis, diagnosis and treatment, and drug resistance of breast cancer, as well as guiding the treatment and prognosis of patients. However, benefits are poor, and relevant molecular mechanisms of action are limited.
目的 研究CD14过表达对胃癌细胞核转录因子-κB（NF-κB）活性以及人β防御素-2（hBD-2）表达的影响，探讨CD14在胃癌发生发展中的作用。 方法 体外培养CD14稳定转染的胃癌SGC-7901细胞系及空质粒转染的对照细胞，CD14蛋白受体胞壁酰二肽刺激细胞，凝胶迁移实验检测NF-κB的活性，蛋白质印迹法检测NF-κB蛋白的表达，同时分别用逆转录-聚合酶链反应以及蛋白质印迹法检测hBD-2 mRNA及蛋白的表达。 结果 与对照组相比，CD14过表达的细胞中NF-κB的活性明显增强，蛋白表达量也大幅度增加，同时hBD-2的mRNA及蛋白的表达都有所提高。 结论 胃癌细胞中CD14在介导NF-κB的激活以及hBD-2的表达中发挥重要作用。
Background: The association between CD14-159C/T polymorphism and sepsis has been assessed but results of current studies appeared conflicting and inconstant. This analysis was aimed to determine whether the CD14-159C/T polymorphism confers susceptibility to sepsis or is associated with increased risk of death from sepsis. Method: The authors conducted a comprehensive search of PubMed, EMBASE, ISI Web of Science, Cochrane library, ScienceDirect, Wiley Online Library and CNKI databases according to a prespecified protocol. Language limits were restricted to English and Chinese. Two reviewers independently selected the articles and extracted relevant data onto standardized forms. Disagreements were settled by discussion and suggestions from senior consultants. The strength of association were evaluated by odds ratio (OR) and 95% confidence interval (CI). Studies failed to fit the Hardy-Weinberg-Equilibrium were excluded. Results: The research identified a total of 2317 full-text articles of which 14 articles met the predefined inclusion criteria. Meta-analysis was performed for allele frequency of C versus T, as well as genotypes CC + CT versus TT (dominant model), CC versus TT + CT (recessive model), CT versus TT and CC versus TT (additive model). All control samples were in Hardy-Weinberg proportion. No significant association between CD14-159C/T polymorphism and sepsis susceptibility or mortality were detected in the overall population. Nonetheless, subgroup analysis of Asian ethnicity revealed significant association between the CD14-159C/T polymorphism and susceptibility to sepsis in additive model (CC versus TT: OR = 0.52, 95% CI 0.29-0.92, p = 0.03) and recessive model (CC versus CT + TT: OR = 0.50, 95% CI 0.30-0.84, p = 0.009). Of note, three out of the five papers included in the subgroup focused exclusively on burn ICU patients. Conclusions: This meta-analysis demonstrated that CD14-159C/T polymorphism is likely to be associated with susceptibility to sepsis in Asian population, especially for the TT genotype. However, bias may rise for etiologic reasons because the majority of subjects in the subgroup came from burn ICU. CD14-159C/T polymorphism is not relevant to sepsis mortality in any genetic models, regardless of the ethnicities. Due to the exploratory nature of the study, no adjustment for multiple testing was adopted, and therefore the results should be interpreted with precaution. Well-designed studies with larger sample size and more ethnic groups are required to further validate the results.