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Objective:To investigate the relationship between neutrophil chemotactic function and chemokine receptor in the early stage of deep second- and third-degree burns.Methods:Twenty patients with severe burns (burn group) who received treatment within 6 hours after burns in Yantai Yeda Hospital from January 2019 to June 2020 were included in this study. Twenty healthy controls (healthy group) who concurrently received physical examination in the same hospital were also included. The general data and laboratory examination indexes in each group were analyzed. The correlation between neutrophil chemotactic function and chemokine receptor was evaluated.Results:There were no significant differences in general data between the two groups (all P > 0.05). At 1, 3 and 5 days after admission, the number of neutrophils, the number of white blood cells, and procalcitonin, C-reactive protein, interleukin-6, interleukin-10, and tumor necrosis factor-α levels in the burn group were significantly higher than those in the healthy control groups ( F = 12.56, 13.45, 15.78, 17.83, 22.56, 13.39, 10.82, all P < 0.05). At 1, 3 and 5 days after admission, neutrophil migration distance in the burn group was (1 510.22 ± 108.45) μm, (1 380.90 ± 115.67) μm, (1 026.10 ± 95.48) μm, respectively, which were significantly shorter than (1 944.67 ± 139.20) μM in the healthy control group ( t = 23.44, 25.67, 27.52, all P < 0.05). At 5 days after admission, chemokine receptors 1 and 2 positive rates in the burn group were (47.40 ± 1.76)% and (75.33 ± 2.42)%, respectively, which were significantly lower than (95.24 ± 4.89)% and (97.78 ± 2.10)% in the healthy control groups ( t = 4.92, 5.67, both P < 0.05). Correlation analysis showed that neutrophil migration distance was positively correlated with chemokine receptor expression in patients with deep second- and third-degree burns ( r = 0.72, 0.61, both P < 0.05). Conclusion:Neutrophil chemotactic function and chemokine receptor expression decrease in the early stage of deep second- and third-degree burns.
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Objective To investigate the effect of sitagliptin in the treatment of elderly patients with type 2 diabetes mellitus complicated with coronary heart disease and its influence on Hcy,irisin and chemerin.Methods From January 2015 to June 2016,600 elderly patients with type 2 diabetes mellitus complicated with coronary heart disease in the Sixth People's Hospital of Cixi were selected and divided into observation group and control group,with 300 cases in each group.The control group received metformin treatment,the observation group was given sitagliptin combined with metformin.Before and after treatment,the blood FBG,HbA1c and BMI,Hcy,irisin and chemerin levels were detected.Results After treatment,the FBG,HbA1 c and BMI levels in the observation group were significantly lower than those in the control group [(6.28 ± 1.43) mmol/L vs.(7.03 ± 1.04) mmol/L,t =5.256;(6.17 ± 1.02) ％ vs.(7.02 ± 0.98) ％,t =7.446;(21.03 ± 2.04) kg/m2 vs.(23.02 ± 1.23) kg/m2,t =14.469] (all P ＜ 0.05).The level of Hcy in the observation group after treatment was significantly lower than that in the control group [(7.48 ± 1.03) μmol/L vs.(10.38 ± 1.74) μmol/L,t =17.868,P ＜ 0.05].After treatment,the blood irisin level in the observation group was significantly higher than that in the control group [(3.28 ± 0.89) μg/mL vs.(2.43 ± 0.38)μg/mL,t =15.213,P ＜ 0.05].After treatment,the chemerin level in the observation group was significantly lower than that in the control group [(210.38 ± 9.84)ng/mL vs.(231.38 ± 10.03)ng/mL,t =24.379,P ＜ 0.05].Conclusion Sitagliptin in the treatment of elderly patients with type 2 diabetes mellitus complicated with coronary heart disease can effectively regulate the levels of Hcy,irisin and chemerin,and improve the curative effect.
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Chemokines and their receptors play an important role in the occurance and development of hepatocellular carcinoma(HCC).The effects of chemokines and their receptors in HCC are different,chemokines and their receptors associated with HCC are mostly expressed in promoting tumor cell proliferation,angiogenesis and invasion,but some chemokines and their receptors play an anti-tumor role.This reviews focus on the role of chemokines and their receptors in HCC.
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Objective To study the effect of rhBNP on serum chemerin and IL-37 levels in acute myocardial infarction (AMI) patients undergoing emergency PCI.Methods Eighty AMI patients who underwent emergency PCI were randomly divided into cortrol group (n =40) and rhBNP treatment group (n=40).The patients in control group were treated with conventional drugs and those in rhBNP treatment group were treated with intravenous rhBNP.Their serum chemerin and IL-37 levels were measured by ELISA.Their LVEDD and LVEF were compared.Results The serum level of chemerin was significantly lower while that of IL-37 was significantly higher in two groups at 72 h and on day 7 after PCI than before PCI (P＜0.05).The serum level of chemerin was significantly lower while that of IL-37 was significantly higher in rhBNP group than in control group at 72 h and on day 7 after PCI (P＜0.05).The LVEDD was significantly shorter while the LVEF was significantly higher in two groups on day 7 and month 1 after PCI than before PCI (P＜0.05).The LVEDD was significantly shorter in rhBNP group than in control group on day 7 and month 1 after PCI (P＜0.05).Conclusion rhBNP can effectively reduce the serum chemerin level,increase the serum IL-37 level,and improve the cardiac function in AMI patients following emergency PCI.The effect of rhBNP is better than that of conventional drugs in AMI patients after emergency PCI.
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Objective To evaluate the effects of Treponema pallidum (T.pallidum) on the expression of chemokine ligands (CXCL) in human brain microvascular endothelial cells (HBMECs).Methods HBMECs were randomly divided into 4 groups,which were treated with viable T.pallidum suspension (T.pallidum group),heat-inactivated T.pallidum suspension (inactivated T.pallidum group),200 μg/L lipopolysaccharide (LPS group) and cell culture medium (blank control group),respectively,for 6,12 and 24 hours.Fluorescence-based quantitative PCR and enzyme-linked immunosorbent assay (ELISA) were performed to determine the mRNA and protein expression of CXCL6,CXCL8 and CXCL10 in HBMECs in the above groups respectively.Transwell migration assay was conducted to evaluate the effects of T.pallidum-stimulated HBMECs on the chemotaxis of human promyelocytic HL-60 leukemia cells (HL-60 cells).Results At 6,12 and 24 hours,the T.pallidum group showed significantly higher mRNA expression of CXCL6,CXCL8 and CXCL10 in HBMECs compared with the blank control group and inactivated T.pallidum group (all P ＜ 0.05),while there were no significant differences between the blank control group and inactivated T.pallidum group (all P ＞ 0.05).Compared with the LPS group,the T.pallidum group showed significantly decreased mRNA expression of CXCL6 and CXCL8 (P ＜ 0.05),but similar mRNA expression of CXCL10(P ＞ 0.05)at 6,12 and 24 hours.At these time points,the levels of CXCL6 and CXCL8 in the culture supernatant of HBMECs were significantly higher in the T.pallidum group than in the blank control group and the inactivated T.pallidum group (all P ＜ 0.05),but no significant differences were observed between the blank control group and the inactivated T.pallidum group (both P ＞ 0.05).Moreover,there were no significant differences in the level of CXCL10 in the culture supernatant of HBMECs among the T.pallidum group,the inactivated T.pallidum group and the blank control group (all P ＞ 0.05).The number of migratory HL-60 cells in the lower Transwell chambers was significantly higher in the T.pallidum group than in the inactivated T.pallidum group and the blank control group (both P ＜ 0.05).Conclusion Viable T.pallidum can up-regulate the gene expression of CXCL6,CXCL8 and CXCL10 in HBMECs,promote the secretion of CXCL6 and CXCL8,and enhance the chemotactic effect of HBMECs on HL-60 cells,which may play a certain role in the occurrence of neurosyphilis.
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Objective To construct the pEGFP-C1-CXCL1 eukaryotic expression vector and to investigate the effect of CXCL1 on the proliferation of HepG2 cells under endoplasmic reticulum stress ( ERS).Methods Fragments of CXCL1 were obtained from the cDNA library of HepG2 cells before CXCL1 was cloned into a pEGFP-C1 vector for a recombinant plasmid pEGFP-C1-CXCL1 which was screened and identified by PCR and sequence alignment .Then,the recombinant plas-mid of pEGFP-C1-CXCL1 was transfected into human 293 T cell line and the expression of CXCL 1 was detected by fluores-cence microscopy and Western blotting.pEGFP-C1-CXCL1was furhter transfected into HepG2 cells, and CCK8 was used to detect the inhibitory effect of CXCL1 on tumor proliferation induced by TM in hepatocellular carcinoma .Results pEGFP-C1-CXCL1 was vertified by sequencing analysis .Fluorescence microscopy showed that pEGFP-C1-CXCL1 was transfected into 293T.CXCL1 expression was detected by Western blotting .CCK8 showed that TM inhibited tumor proliferation , while overexpression of CXCL1 decreased the inhabitory rate on cell proliferation of HepG 2 cells under ER stress compared to pEGFP-C1 group and the control group .Conclusion A recombinant pEGFP-C1-CXCL1 plasmid is successfully constructed that can be expressed stably in human 293T cells.Overexpression of CXCL1 can effectively reduce the inhabitory rate of HCC cells induced by the ER stress.
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Objective@#To explore the plasma chemokines expressions and related clinical implication in patients with Stanford type A aortic dissection (AD).@*Methods@#We retrospectively analyzed the data of 65 patients with Stanford type A aortic dissection, hypertensive patients and 11 healthy subjects admitted in our department from October 2013 to December 2014, they were divided into four groups: NH-CON group (11 healthy subjects), H-AD group (29 AD patients with hypertension), NH-AD group (21 AD patients without hypertension), and H-CON group (14 hypertension patients). Four plasma samples from AD patients and 4 plasma samples from healthy subjects were collected randomly with random numbers table, and the levels of different chemokines were examined by protein array analysis. Then, plasma levels of chemokines including macrophage inflammatory protein 1β(MIP-1β), epithelial neutrophil activating peptide 78(ENA-78), interleukin 16(IL-16), interferon inducible protein 10(IP-10) and FMS-like tyrosine kinase 3(Flt-3) ligand were analyzed by luminex. Pearson analysis was used to determine the correlations between the chemokines and serum C reactive protein (CRP) levels.@*Results@#Plasma levels of MIP-1β(34.0(29.3, 47.2) ng/L vs. 51.0(28.2, 80.7) ng/L, P<0.05) and ENA-78(110.5(59.1, 161.4) ng/L vs. 475.7(299.3, 837.3) ng/L, P<0.05) were significantly lower in H-AD group, while plasma IL-16 level was significantly higher in H-AD group(54.7(16.3, 187.8) ng/L vs. 17.5(11.9, 20.8) ng/L, P<0.05) than in H-CON group. Plasma levels of MIP-1β(48.3(26.4, 62.1) ng/L, P<0.05) were significantly lower in H-AD patients than in NH-AD patients. Plasma level of ENA-78 was significantly lower in NH-AD group than in NH-CON group (95.0(58.0, 155.0) ng/L vs. 257.7(85.2, 397.8) ng/L, P<0.05). The levels of IP-10 and Flt-3 ligand were similar among the 4 groups (all P>0.05). Pearson analysis showed that there were no correlation between MIP-1β(r2=0.01, P>0.05), ENA-78(r2=0.02, P>0.05), IL-16(r2=0.02, P>0.05), IP-10(r2=0.00, P>0.05), Flt-3 ligand(r2=0.02, P>0.05) and CRP levels in patients with Stanford type A aortic dissection.@*Conclusions@#Lower plasma levels of MIP-1β and ENA-78 and higher plasma levels of IL-16 may associate with the occurrence and development of type A aortic dissection, but their concentrations are not correlated with serum CRP levels. There is no significant change on plasma levels of IP-10 and Flt-3 in the Stanford type A aortic dissection patients.
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Objective: To investigate the expressions of stromal cell-derived factor-1 (SDF-1) and its receptor chemokine (C-X-C motif) receptor 4 (CXCR4) as well as the microvessel density (MVD) in patients with multiple myeloma, and to explore their effects on the prognosis. Methods: The expressions of SDF-1 and CXCR4 as well as MVD in bone marrow fr o m 7 8 p ati e n ts wi thmul tiple m yelom a an d 3 0 norm alperson s wered e te ctedby immunohistochemical method. The correlations of age, gender, international staging system (ISS) staging, immunoglobulin typing, light chain classification, SDF-1 expression, CXCR4 expression and MVD with the prognosis of multiple myeloma patients were analyzed. Results: The expression of SDF-1 in bone marrow of multiple myeloma patients was positively cor re lated wi th th e exp ressionof CXCR4 and the count of MVD (b oth P 0.05). The overall survival rate and progression-free survival rate of multiple myeloma patients with low expressions of SDF-1 and CXCR4 were lower than those of patients with high expressions of SDF-1 and CXCR4 (both P < 0.05). The overall survival rate and progression-free survival rate of patients with multiple myeloma in low count of MVD group were higher than those in the high count of MVD group (both P < 0.05). The age, SDF-1 and CXCR4 expressions, and MVD were independent prognostic factors for the patients with multiple myeloma (all P < 0.05). Conclusion: The expressions of SDF-1 and CXCR4 and the count of MVD were independent prognostic factors for the patients with multiple myeloma. SDF-1, CXCR4 and MVD may play promoting roles in the malignant progression of multiple myeloma, so they are expected to become new targets for the treatment of multiple myeloma in the future.
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Objective: To investigate the effects of local injection of Duffy antigen receptor for chemokines (DARC) protein on the growth of lung adenocarcinoma A549 xenografts in nude mice and the angiogenesis in xenograft tumor tissues. Methods: The lung cancer xenograft model was established by using lung adenocarcinoma A549 cells. After xenograft formation, the different doses (l, 10 and 100 ng) of DARC protein were injected into the xenografts as the low, medium and high dose groups, respectively; while 0.9% sodium chloride solution (100
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Objective To investigate the effects of ARHI transfection on the chemokines and receptors related gene expression profile of PANC1 cells.Methods Plasmids expressing ARHI and empty plasmid were transfected into PANC1 cells, and the stably expressed cell lines were established by using G418.mRNA expression of chemokines and receptors related genes was detected by PCR Array.Real-time PCR was used to detect mRNA expression of the genes related vascular growth.Results In cells transfected with ARHI gene, the expression levels of mRNA of 36 genes were down-regulated, and 9 were up-regulated.Among the genes related to tumor metastasis and invasion CXCL12 and CXCR4 were significantly down-regulated (6 folds).Among the genes related to the localization of distant organ infiltration and latency, CXCL12, CXCR4 and CCR7 were significantly down-regulated,and CXCR5 was slightly down-regulated.Among the gene with tumor immunity,CXCL8,CXCR1 and CCR7 were significantly down-regulated.Gene expression of CXCL1,CXCL8,CXCR4 and CXCR3 detected by Real-time PCR were consistent with PCR array.Conclusions ARHI gene inhibits the expression of chemokines and receptors related to tumor metastasis,angiogenesis and tumor immunity.
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Objective To investigate the effects of interleukin (IL)-34 on the proliferation and chemokines expression of fibroblast-like synoviocytes (FLS) in patients with rheumatoid arthritis (RA).Methods RA FLS were isolated and cultured in the presence or absence of IL-34.FLS proliferation was determined by methyl thiazlyl tetrazoliu method (MTT) method.The levels of chemokines from RA FLS supernatant were detected by protein chip AAH-CYT-G1000 assay.The IL-34 receptor (IL-34R) expression on RA FLS was analyzed by flow cytometry (FCM).Statistical analysis between groups was performed by t test.Results Compared to the control group, the proliferation of IL-34-stimulated RA FLS was obviously increased, and up to the maximum at 72 hours.In addition, the levels of chemokines [epithelial neutrohil-activating peptide 78 (ENA-78), IL-8, growth-related oncogene (GRO), macrophage chemoattractant protein-1 (MCP-1)] on RA FLS supernatant in IL-34 stimulated group were significantly elevated than those in the control group [ENA-78: (397.1±8.2) pg/ml, (54.0±2.9) pg/ml (t=127.61, P＜0.01);IL-8:(2 017±36) pg/ml, (778±102) pg/ml (t=36.67, P＜0.01);GRO: (4 935±160) pg/ml, (2 746±188) pg/ml (t=43.60, P＜0.01);MCP-1: (46 798±1 293) pg/ml, (27 813±2 329) pg/ml (t=22.43, P＜0.01)].IL-34R was highly expressed on the RA FLS.Conclusion IL-34 promotes RA FLS proliferation and chemokines expression, which may be one of the important mechanisms involved in the pathogenesis of RA.
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Chemokines and chemokine receptors involve in biological activity and pathological process widely.It has been reported that many tumor cells overexpress functional chemokines.In lung cancer,chemo-kines involve in its proliferation,apoptosis,invasion and metastasis.Chemokines and chemokine receptor over-expressed in lung cancer can be used as specific target for pertinent anti-tumor treatment.
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Objective To detect the expression levels of multiple serum chemokines including IFN-inducible T cell chemoattractant (ITAC),Fractalkine,macrophage inflammatory protein (MIP)-3α,IL-8,MIP-lα,MIP-1β in patients with lung cancer and explore their association with the clinical characteristics of lung cancer as well as the correlations among these chemokines.Methods Forty newly diagnosed patients with lung cancer and thirty healthy controls were enrolled for detection of the serum levels of 6 kinds of chemokines by Luminex technology.The correlations of clinical characteristics of lung cancer with these chemokines and the correlations among these chemokines were analyzed by SPSS 17.0 software.Results The serum levels [M (QR)] of IL-8,Fractalkine and MIP-3α in patients with lung cancer were 5.16 (4.74),128.45 (141.89),10.31 (8.88) respectively,and 2.01 (0.95),61.46 (74.81),8.08 (5.87) respectively in control group,with significant differences (Z =-4.783,P ＜0.001;Z =-4.046,P ＜0.001;Z =-3.105,P =0.002).The expression of MIP-1β in lung adenocarcinoma was significantly higher than that in squamous carcinoma [18.32 (12.27) vs.13.72 (7.31),Z =-2.212,P =0.027],and of ITAC in squamous carcinoma was significantly higher than that in small cell lung cancer [24.51 (22.48) vs.9.28 (4.85),Z =-2.460,P =0.014].The expressions of MIP-3α and Fractalkine were positively correlated in the two groups (r =0.619,P＜0.001;r=0.766,P＜0.001).Conclusion The expressions of IL-8,Fractalkine and MIP-3α increase significantly in lung cancer patients,and they are may play important roles in metastatic lung cancer.
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Objective To investigate the effect of hyperbaric oxygen on the expression of fractalkine (FKN) in the nerve tissues of rats with neuropathic pain (NP).Methods Thirty-two male Sprague-Dawley rats, weighing 250-280 g, aged 10-12 weeks, were divided into 4 groups (n=8 each) using the random number table: control group (group C), sham operation group (group S), group NP, and hyperbaric oxygen group (group H).NP was induced by chronic constriction injury (CCI) in anesthetized rats.The left sciatic nerve was exposed, and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 silk thread.Group H received hyperbaric oxygen therapy once a day for 5 consecutive days starting from day 1 after CCI.The rats were placed into the hyperbaric oxygen chamber, which was pressurised to 2 atmosphere absolute at a rate of 10 kPa/min, and maintained at this level for 60 min.The pressure was then decreased to the normal pressure at a rate of 10 kPa/min.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before CCI, and 3, 5, 7 and 14 days after CCI.After measurement of pain threshold at 3 and 7 days after CCI, 4 rats were selected and sacrificed.The sciatic nerve and lumbar segment of the spinal cord were removed for determination of the expression of FKN by Western blot.Results Compared with group C, the MWT was significantly decreased, and TWL was shortened at each time point after CCI, the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was upregulated in group NP (P＜0.05) , and no significant change was found in the parameters mentioned above in group S (P＞0.05).Compared with group NP, the MWT was significantly increased, and TWL was prolonged at each time point after CCI, and the expression of FKN in the sciatic nerve at 3 days after CCI, and in the sciatic nerve and spinal cord at 3 and 7 days after CCI was down-regulated in group H (P＜0.05).Conclusion The mechanism by which hyperbaric oxygen mitigates NP is related to inhibition of over-expression of FKN in the nerve tissues of rats.
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BACKGROUND:Previous studies have indicated that resistin stimulates a large set of chemokines in chondrocytes that are known to be important in inflammatory joint lesions. OBJECTIVE:To further investigate the mechanism of co-regulation roles of transcription and post-transcription in the up-regulation of two chemokine genes CCL3 and CCL4 in chondrocytes in response to resistin. METHODS:Human chondrocytes, T/C-28a2 and ATDC5 cels were cultured. The function of resistin on the chemokine genes, and the expression of C/EBPβ, nuclear factor-κB isoforms and chondrogenic specific miRNAs were tested by qPCR. The co-regulation of C/EBPβ and nuclear factor-κB was investigated by nuclear factor-κB inhibitor (IKK-NBD) and C/EBPβ inhibitor (SB303580) treatments, and subcelular localization was detected with or without resistin stimulation. RESULTS AND CONCLUSION:Resistin could increase the expression of chemokine genes independently. Chondrocytes reacted in a non-restrictedly cel-specific manner to resistin; C/EBPβ inhibitor, nuclear factor-κB and some chondrogenic specific miRNAs in a combinatorial manner regulated chemokine gene expression. The activity of C/EBPβ was augmented by a transient increase in activity of nuclear factor-κB, and both transcription factors acted independently on the chemokine genes, CCL3 and CCL4.
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Objective To establish experimental autoimmune thyroiditis (EAT) rat model induced by bovine thyroglobulin (bTg) and to observe the effect of iodine on IP-10 in rat serum and IP-10 mRNA expression in rat thyroid tissue.Methods One hundred and thirty-five four-week old female Lewis rats were divided into normal control (NC,20 rats) group;TG group,25 rats;H Ⅰ group,20 rats;H Ⅰ + TG group,25 rats;H Ⅱ group,20 rats and H Ⅱ + TG group,25 rats according to a random number table.The water iodine concentration was 25.7 μg/L given to rats of HⅠ and H I + TG groups,and 423.3 μg/L of H Ⅱ and H Ⅱ + TG groups.Rats of NC and TG groups drank distilled water.Rats of TG,H Ⅰ + TG,H Ⅱ + TG groups were immunized with 0.1 ml bTg (8 g/L) in IFA.All rats were killed at the end of 15 weeks.Urinary iodine was determined by As3+-Ce4+ catalytic spectrophotometry (WS/T 107-2006).Pathological changes in thyroid tissue were observed by light microscope.Serum IP-10 was determined by enzyme-linked immunosorbent assay (ELISA),and IP-10 mRNA expression in thyroid was detected by real-time PCR.Results The differences of urinary iodine between groups were statistically significant (x2 =106.4,P ＜ 0.05).Compared with NC group (456.45 μg/L) urinary iodine in other groups increased significantly (TG,H Ⅰ,H Ⅰ + TG,HⅡ,HⅡ + TG:800.08,18 633.20,13 869.08,87 889.97,61 661.51 μg/L,all P ＜ 0.05).The pathological changes of rats in each group aggravated following increased iodine intake,NC group had normal thyroid structure;thyroid of TG group had a small amount of lymphocytes;thyroid of H Ⅰ group showed irregular follicular,part of the follicular was destroyed;a large number of lymphocytes infiltrated between follicular of H Ⅱ group;in H Ⅱ + TG group,the follicular was destroyed severely,diffuse inflammatory cell infiltration.The difference of serum IP-10 between groups no were statistically significant (F =1.462,P ＞ 0.05).The expression of IP-10 mRNA of H Ⅰ + TG (2.80 ± 1.73) rats thyroid was higher than that in NC (1.65 ± 1.62) and H Ⅰ (1.07 ± 1.00) groups,H Ⅱ (0.64 ± 0.64),H Ⅱ + TG (0.80 ± 0.49) were lower than H Ⅰ + TG group (all P ＜ 0.05).Conclusions Excessive iodine intake could have increased inflammatory cells in EAT rat and rats have showed more serious pathologic changes.These phenomena may be ralated with changed expression of IP-10 mRNA in EAT rat thyroid.
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The chemokine CXCL12 and its receptor CXCR4 played a very important role in the gastric carcinoma,which promoted the growth,invasion,and metastasis of the gastric carcinoma through various of signal pathways.In this paper,the literatures related CXCL12,signal pathways and gastric carcinoma were retrieved and explored.And the authors present the research progress concerning the roles of CXCL12 and its regulating mechanism in neoplasm,especially in gastric cancer.
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Chemokine CCL18 plays significant roles in immune regulation by recruiting of inflammatory cells,which involves in immune and inflammatory processes.CCL18 protein is overexpressed in the serum of patients with cancer and some tumor tissues.However,it is still controversial that CCL18 plays the role of tumor promoter or tumor suppressor.Researches on the roles and mechanisms of CCL18 can provide new target for diagnosis and treatment of cancer.
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Objective To investigate the association between the signaling pathways of MCP-1-pCDH-GFP-trans?fected cells and deep venous thrombosis (DVT). Methods The cultured human umbilical vein endothelial cells (HUVECs) were tested by immunofluorescence and co-immunoprecipitation methods. The constructed MCP-1 over-expression/interfer?ence vector, and the change of transcription profile were detected by microarray assay and biological information technology analysis. Results MCP-1 over-expression/interference vector MCP-1-pCDH-GFP/MCP-1-LMP shRNAmir1 was con?structed and HUVECs were transfected. According to the microarray analysis we found that there were 18 down-expressed signaling pathways and 7 up-expressed signaling pathways in MCP-1-pCDH-GFP-transfected cells. There were 60 down-expressed signaling pathways and 15 up-expressed signaling pathways in the MCP-1-LMP shRNAmir1 transfected cells. Conclusion Signaling pathways of MCP-1 plays an important role in DVT formation,which may provide us a new way to study molecular mechanism of DVT.
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BACKGROUND:Previous studies have shown that different doses of ionizing radiation may have some impact on maturation and immune function of dendritic cells. OBJECTIVE:To evaluate the effect of 18 F-FDG with different concentrations on maturation and immune function of dendritic cells from human peripheral blood mononuclear cells in vitro. METHODS:Human peripheral blood mononuclear cells-derived mature dendritic cells were divided into five groups:PBS, 92.5×10 4, 185×104, 370×104, 740×104 Bq/mL 18 F-FDG were separately added into each group. Dendritic cells were col ected 24 hours later. Apoptosis rate, phenotypic expression (CD1α, CD80, CD83, CD86, HLA-DR), ability of mixed lymphocyte reaction and expression of macrophage inflammatory protein 1αand monocyte chemotactic factor-1 in cellculture supernatant were detected. RESULTS AND CONCLUSION:Apoptosis rate, phenotypic expression of CD86, ability of mixed lymphocyte reaction and expression of monocyte chemotactic factor-1 were down-regulated after culture in 740×10 4 Bq/mL 18F-FDG. However, 18F-FDG at other concentrations had no influence on maturation and immune function of dendritic cells. This study demonstrates that low-concentration 18F-FDG has little influence on apoptosis, maturation, antigen presentation, and migratory capacity of dendritic cells, and it may be selected at an appropriate concentration as a label for dendritic cells in vitro.