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Objective To investigate the relieving effects of knockdown of long non-coding RNA(lncRNA)taurine up-regulated gene 1 (TUG1) on inhibiting nucleotide binding oligomerization domain like receptor protein 1 (NLRP1) inflammasome and the progression of Alzheimer’ s disease. Methods Wild-type (WT group, 10 mice) or amyloid precursor protein (APP) / presenilin-1 (PS1) transgenic mice (30 mice) with a genetic background of C57 / BL6 aged 9-10 weeks were used in this study. APP / PS1 transgenic mice were randomly divided into model group, model+lncRNA TUG1 short hairpin RNA (shRNA) group and model + shRNA non target (NT) group (n = 10) . Blood samples, cerebral cortex tissues, primary microglial cells and primary astrocytes were collected from mice 12 weeks of age on day 1 (3-month-old) and 32 weeks of age on day 1 (8-month-old), with 5 mice per group at each time point. Real-time PCR analysis was used to detect the expression levels of lncRNA TUG1 and macrophage migration inhibitory factor (MIF) mRNA in cerebral cortex tissues and primary microglial cells, and C1r and C1s mRNA levels in primary astrocytes of 3-month-old and 8-month-old mice in the above 4 groups, respectively. ELISA was used to determine the MIF in plasma samples of the above 4 groups of mice. Primary microglia and astrocytes from the cerebral cortex of 3-month-old and 8-month-old mice were co-cultured. CCK-8 method was used to determine the proliferation ability of the above cells. Western blotting was used to determine the expression levels of MIF, pro interleukin-1β (pro-IL-1β), apoptosis associated speck-like protein containing a caspase recrult domain(ASC), Caspase-1 (p20), Caspase-1 (full), NLRP1 and NLRP3 in cerebral cortex tissues of 3-month-old and 8-month-old mice. Immunofluorescent staining was used to determine amyloid beta(Aβ) in cerebral cortex of 8-month-old mice. Results At the age of 3-month-old and 8-month-old, compared with the WT group, the relative expression level of lncRNA TUG1 and MIF in cerebral cortex tissues and primary microglia of model group mice was significantly up-regulated, with primary microglial cells and astrocytes proliferation ability enhanced (P0. 05) . There was no significant difference between the model group and the model+shRNA NT group mice of all the above factors (P>0. 05) . Conclusion In APP / PS1 transgenic mice, up-regulation of lncRNA TUG1 and MIF are positively associated with the activation of NLRP1 inflammasome in mice cerebral cortex tissues and primary microglia. Knock-down of lncRNA TUG1 can ameliorate the progression of Alzheimer’ s disease.
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Background: Psoriasis is associated with significant morbidity and impaired quality of life. Identification of the host genes that influence disease susceptibility and can potentially guide future, targeted therapy is the need of the hour. Aims: The aim of the study was to investigate the associations of macrophage migration inhibitory factor (MIF) gene polymorphisms, that is, a 5–8-CATT tetra nucleotide repeats at -794 (-794*CATT5–8) and a single-nucleotide polymorphism at -173 (-173*G/C) with the risk of chronic plaque psoriasis and to observe the correlation, if any, of disease determinants with genetic functional variants and circulating MIF levels. Methods: Five hundred and seventeen individuals (265 psoriasis patients and 252 controls) were genotyped for MIF gene polymorphisms. Data were analyzed with respect to disease susceptibility, serum MIF levels, disease severity, age at onset, disease duration and presence of comorbidities. Results: The presence of co-morbidities was more frequently noted in patients with late onset disease (P = 0.01). No statistically significant differences were observed either in genotype (P = 0.680) or allele frequency (P = 0.69) with respect to distribution of MIF-173*G/C polymorphism between patients and controls. The frequencies of genotypes -794*CATT 5/7 and 7/7 were significantly lower in patients (P = 0.027* and 0.038*, respectively). CATT*5/MIF-173*C haplotype occurred at a higher frequency in patients (odds ratio 3.03, 95% confidence intervals 1.09–8.47, P = 0.02). The mean serum MIF levels were significantly higher in patients as compared to controls (P < 0.001). The presence of either extended MIF -794*CATT repeats or C allele did not reveal any significant association with serum MIF levels or age at onset. Analysis of effect of various disease determinants revealed no significant association with genetic variants and serum MIF levels. Limitations: The lesional expression of MIF could not be studied. Conclusion: Our results showed that CATT*5/MIF-173*C haplotype is associated with increased susceptibility to psoriasis vulgaris.
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Macrophage migration inhibitory factor (MIF) is an enzyme-active pleiotropic cytokine that is expressed in various immune cells and tumor cells. MIF plays diverse roles in inflammation and tumor progression. It acts as a cytokine involved in immune response and inflammatory lesions. Additionally, MIF is closely associated with tumor proliferation, metastasis, and other tumor hallmarks, exerting a multifaceted influence on tumor occurrence and progression. MIF not only functions by being secreted into the extracellular space as a cytokine but can also be localized within the cytoplasm and nucleus, exhibiting diverse biological functions. As MIF in promoting tumor progression becomes increasingly recognized, MIF-based therapeutic strategies have become a hot research topic in oncology. Here, we provide a comprehensive review of MIF with different subcellular localization about their pro-tumoral functions. A better understanding of MIF in tumor biology will bring broader perspectives for the development of novel MIF targeting strategies and give promising direction for future tumor treatments.
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There is still a serious challenge of the measurement of critical quality attributes (CQAs) related to clinical efficacy for Chinese materia medica manufacturing. To overcome this challenge, an integrated strategy of biosensor and ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) was proposed using Tongren niuhuang qingxin pills as a trial. Firstly, an original biosensor was created using a semiconductor chip material high electron mobility transistor (HEMT) as the transducer and the macrophage migration inhibitory factor (MIF) as the identification element. By this MIF-HEMT biosensor, the efficacy on stoke of different components from Tongren niuhuang qingxin pills was measured. It was clear that all three components of Tongren niuhuang qingxin pills had strong therapeutic effects on stroke, especially the section A, the KD of which reached to 8.722×10-10 g·mL-1. Furthermore, MIF-HEMT biosensor integrated UPLC-MS/MS was introduced to identify the efficacy CQAs of different components of Tongren niuhuang qingxin pills. As a result, 19 potential CQAs, such as albiforin, paeoniflorin, and prim-O-glucosylcimifugin, were measured as the efficacy CQAs of Tongren niuhuang qingxin pills on stroke treatment by MIF. These results provided vital measurement techniques and methodological guidance for the CQAs study of Tongren niuhuang qingxin pills intervention in MIF-induced stroke treatment. This also provided an essential guideline for the efficient utilization and quality control measurement of high-quality classical recipes.
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@#Parthanatos is a form of programmed cell death,which is also known as poly(ADP-ribose)polymerase 1(PARP1)-mediated apoptosis-inducing factor(AIF)and macrophage migration inhibitory factor(MIF)-dependent cell death according to its molecular mechanism. Parthanatos is the main cause of a variety of neurodegenerative diseases,such as Parkinson's disease(PD),Alzheimer's disease(AD),motor neuron disease,and is also involved in the pathogenesis of some tumors,such as lung cancer and breast cancer. Therefore,a thorough understanding of the molecular mechanism of Parthanatos is crucial for the therapeutic strategies of related diseases. In recent years,studies have found that effective regulation of the occurrence of Parthanatos by regulating the key proteins PARP1,AIF and MIF is expected to become a therapeutic target for many diseases. Based on the specific molecular mechanism of Parthanatos,this paper reviewed the research progress of therapeutic strategies for related diseases from the aspects of inhibiting and promoting Parthanatos.
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Objective To investigate the effect of Trichomonas vaginalis macrophage migration inhibitory factor (TvMIF) on THP-1 macrophages.. Methods Recombinant TvMIF protein was prokaryotic expressed and purified, and endotoxin was removed after identification. Following exposure to TvMIF at concentrations of 0, 1, 5, 10, 50 and 100 ng/mL, the cytotoxicity of the recombinant TvMIF protein to THP-1 macrophages was tested using cell counting kit (CCK)-8 assay, and the apoptosis of THP-1 macrophages and reactive oxygen species (ROS) were detected using flow cytometry. The relative expression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), caspase-1, interleukin-1β (IL-1β) and IL-18 genes was quantified using real-time fluorescent quantitative PCR (qPCR) assay, and the expression of caspase-1, NLRP3, gasdermin D (GSDMD), gasdermin D N-terminal (GSDMD-NT) and pro-IL-1β proteins were determined using Western blotting assay. Results Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) displayed successful expression and purification of the recombinant TvMIF protein with a molecular weight of 15.5 kDa, and the endotoxin activity assay showed the successful removal of endotoxin in the recombinant TvMIF protein (endotoxin concentration < 0.1 EU/mL), which was feasible for the subsequent studies on protein functions. Flow cytometry revealed that the recombinant TvMIF protein at a concentration of 10 ng/mL and less promoted the apoptosis of THP-1 macrophages, and the highest apoptotic rate of THP-1 macrophages was seen following exposure to the recombinant TvMIF protein at a concentration of 5 ng/mL, while the recombinant TvMIF protein at concentrations of 50 and100 ng/mL inhibited the apoptosis of THP-1 macrophages. Exposure to the recombinant TvMIF protein at a concentration 1 ng/mL resulted in increased ROS levels in THP-1 macrophages. qPCR assay quantified significantly elevated caspase-1, NLRP3, IL-18 and IL-1β expression in THP-1 macrophages 8 hours post-treatment with the recombinant TvMIF protein at a concentration 1 ng/mL, and Western blotting determined increased caspase-1, NLRP3, pro-IL-1β, GSDMD and GSDMD-NT protein expression in THP-1 macrophages following exposure to the recombinant TvMIF protein at a concentration 1 ng/mL. Pretreatment with MCC950 significantly reduced GSDMD and GSDMD-NT protein expression. Conclusions High-concentration recombinant TvMIF protein inhibits macrophage apoptosis, while low-concentration recombinant TvMIF protein activates NLRP3 inflammasome and promotes macrophage pyroptosis.
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Objective:To investigate the effects of macrophage migration inhibitory factor (MIF) on AMPK/ERK/mTOR autophagy signaling pathway in primary human umbilical vein endothelial cells (HUVEC) after dengue virus type 2 (DENV2) infection.Methods:The virulence of DENV2 to C6/36 cells was assessed with 50% tissue culture infectious dose (TCID 50). NS1 gene fragments in DENV2-infected HUVEC were detected by RT-PCR. Transmission electron microscopy was used to detect autophagosomes. Western blot was performed to detect the effects of DENV2 infection on the expression of autophagy-related protein LC3-Ⅱ and MIF in HUVEC. The correction of MIF with LC3-Ⅱ was then analyzed. HUVEC were pretreated with MIF inhibitor (ISO-1) or pathway inhibitor (Compound C or U0126), and then the changes in the expression of MIF, adenosine 5′-monophosphate-activated protein kinase (AMPK) pathway-related proteins and LC3-Ⅱ after DENV2 infection were detected by Western blot to reveal the correlation between MIF and AMPK autophagy pathway. Results:The TCID 50 to C6/36 cells was 10 -9.09/ml in this experiment. NS1 gene fragments were detected in DENV2-infected HUVEC. Autophagosomes or autophagolysosomes were observed in the infected HUVEC and there were differences in autophagy induced by different doses of DENV2. The mRNA levels of MIF and LC3-Ⅱ in HUVEC were positively correlated after DENV2 infection. MIF inhibitor affected AMPK, ERK and LC3-Ⅱ levels, but had no significant influence on MIF expression at protein level. Conclusions:MIF could affect autophagy through regulating the AMPK/ERK/mTOR signaling pathway in HUVEC during DENV2 infection.
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Macrophage migration inhibitory factor (MIF) is a widely expressed multipotent cytokine that participates and plays an important role in various inflammatory and immune diseases‚ and is a biomarker or therapeutic target of many diseases. MIF is highly conserved in phylogeny and there are specific binding sites of various transcription factors in its promoter region‚ which can regulate the expression of MIF. MIF functions both inside and outside cells‚ and MIF is constitutively expressed. Therefore‚ it is of great significance to study the related factors that regulate MIF gene expression and stimulate MIF secretion. This article summarizes and classifies the related factors affecting MIF gene expression by briefly describing the binding sites on the MIF gene and MIF promoter. According to the way of binding with the MIF gene‚ it can be divided into:(1) binding to specific sites of MIF gene promoters to change transcription activity; (2) binding to MIF CATT5-8 microsatellite repeats to change highly expressed MIF alleles (3) non-coding RNAs regulating MIF expression; (4) related factors affecting MIF secretion. By reviewing the four types of related factors that regulate MIF gene expression‚ we will understand the regulatory mechanism and influencing factors of MIF gene expression‚ in order to provide a theoretical basis for its treatment of related diseases.
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Niño , Humanos , Alanina Transaminasa , Alelos , Azatioprina , Biopsia , Enfermedad Crónica , Diagnóstico , Fibrosis , Genotipo , Hepatitis Autoinmune , Hígado , Macrófagos , Recurrencia , Linfocitos TRESUMEN
Macrophage migration inhibitory factor (MIF), a type of pleiotropic immunoregulatory cytokine with a specific structure, participates in the regulation of host cell growth and migration and immune responses. Following parasitic infections, hosts may produce MIF and then participate in the parasite-host interactions. In addition, parasites may secrete parasite-derived MIF, and they jointly participate in parasite-host interactions. This paper reviews the regulation of MIF gene expression following parasitic infections, the role of MIF in parasite-host immune system interactions, and important signaling pathways of MIF-mediated immune responses.
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Macrophage migration inhibitory factor (MIF), a type of pleiotropic immunoregulatory cytokine with a specific structure, participates in the regulation of host cell growth and migration and immune responses. Following parasitic infections, hosts may produce MIF and then participate in the parasite-host interactions. In addition, parasites may secrete parasite-derived MIF, and they jointly participate in parasite-host interactions. This paper reviews the regulation of MIF gene expression following parasitic infections, the role of MIF in parasite-host immune system interactions, and important signaling pathways of MIF-mediated immune responses.
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Objective@#To investigate the expression of macrophage migration inhibitory factor (MIF) in pulmonary tissues from patients with chronic obstructive pulmonary disease (COPD) and the relationship with its clinical features.@*Methods@#One hundred and eighty patients who underwent pulmonary bullectomy lobectomy due to pneumatocele from January 2015 to September 2018 in Longgang Central Hospital were enrolled and classified into patients without COPD (control group)and patients with COPD (COPD group), with 90 patients each group. According to the lung function parameters, 90 patients with COPD were divided into the mild COPD group, the moderate COPD group, and the severe COPD group. The levels of mRNA and protein of MIF were measured with RT-PCR, ELISA and Western blot. One-way ANOVA, Pearson correlation analysis and SNK-q test were used to analyze the results with SPSS 18.0, and P<0.05 was considered statistically significant.@*Results@#The level of MIF in pulmonary tissues from the control group was obviously lower than those in the COPD group (P<0.05). The level of MIF in pulmonary tissues in the severe COPD group was obviously higher than those in pulmonary tissues in the mild COPD, moderate COPD and control groups (P<0.05). MIF was positively correlated with the lung function parameters (P<0.05).@*Conclusion@#The high expression of MIF in pulmonary tissues is closely related to the severity of COPD.
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Objective To investigate the expression of macrophage migration inhibitory factor (MIF) in pulmonary tissues from patients with chronic obstructive pulmonary disease (COPD) and the relationship with its clinical features.Methods One hundred and eighty patients who underwent pulmonary bullectomy lobectomy due to pneumatocele from January 2015 to September 2018 in Longgang Central Hospital were enrolled and classified into patients without COPD (control group) and patients with COPD (COPD group), with 90 patients each group. According to the lung function parameters, 90 patients with COPD were divided into the mild COPD group, the moderate COPD group, and the severe COPD group. The levels of mRNA and protein of MIF were measured with RT-PCR, ELISA and Western blot. One-way ANOVA, Pearson correlation analysis and SNK-qtest were used to analyze the results with SPSS 18.0, andP<0.05 was considered statistically significant.Results The level of MIF in pulmonary tissues from the control group was obviously lower than those in the COPD group (P<0.05). The level of MIF in pulmonary tissues in the severe COPD group was obviously higher than those in pulmonary tissues in the mild COPD, moderate COPD and control groups (P<0.05). MIF was positively correlated with the lung function parameters (P<0.05).Conclusion The high expression of MIF in pulmonary tissues is closely related to the severity of COPD.
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PURPOSE: The purpose of this study was to identify novel plasma biomarkers for distinguishing nasopharyngeal carcinoma (NPC) patients from healthy individuals who have positive Epstein-Barr virus (EBV) viral capsid antigen (VCA-IgA). MATERIALS AND METHODS: One hundred seventy-four plasma cytokines were analyzed by a Cytokine Array in eight healthy individuals with positive EBV VCA-IgA and eight patients with NPC. Real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry were employed to detect the expression levels of macrophage migration inhibitory factor (MIF) and CC chemokine ligand 3 (CCL3) in NPC cell lines and tumor tissues. Plasma MIF and CCL3 were measured by ELISA in 138 NPC patients, 127 EBV VCA-IgA negative (VN) and 100 EBV VCA-IgA positive healthy donors (VP). Plasma EBV VCA-IgA was determined by immunoenzymatic techniques. RESULTS: Thirty-four of the 174 cytokines varied significantly between the VP and NPC group. Plasma MIF and CCL3 were significantly elevated in NPC patients compared with VN and VP. Combination of MIF and CCL3 could be used for the differential diagnosis of NPC from VN cohort (area under the curve [AUC], 0.913; sensitivity, 90.00%; specificity, 80.30%), and combination of MIF, CCL3, and VCA-IgA could be used for the differential diagnosis of NPC from VP cohort (AUC, 0.920; sensitivity, 90.00%; specificity, 84.00%), from (VN+VP) cohort (AUC, 0.961; sensitivity, 90.00%; specificity, 92.00%). Overexpressions of MIF and CCL3 were observed in NPC plasma, NPC cell lines and NPC tissues. CONCLUSION: Plasma MIF, CCL3, and VCA-IgA combination significantly improves the diagnostic specificity of NPC in high-risk individuals.
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Humanos , Biomarcadores , Western Blotting , Cápside , Línea Celular , Quimiocina CCL3 , Estudios de Cohortes , Citocinas , Diagnóstico , Diagnóstico Diferencial , Ensayo de Inmunoadsorción Enzimática , Herpesvirus Humano 4 , Inmunoglobulina A , Inmunohistoquímica , Macrófagos , Plasma , Reacción en Cadena en Tiempo Real de la Polimerasa , Sensibilidad y Especificidad , Donantes de TejidosRESUMEN
Background: Erythema nodosum leprosum is an immune-mediated complication of leprosy which causes significant morbidity. Biomarkers in the pathogenesis of erythema nodosum leprosum are not yet fully determined. Aim: To determine macrophage migration inhibitory factor levels in the sera of leprosy patients with erythema nodosum leprosum and to correlate the same with clinical parameters. Methods: This cross-sectional study included 37 consecutive leprosy patients with active erythema nodosum leprosum and 31 age- and sex-matched controls. Detailed clinical history and examination findings were recorded including the severity and frequency of erythema nodosum leprosum. Slit skin smears and histopathologic examination were done in all patients at baseline. Serum macrophage migration inhibitory factor levels were determined using an enzyme-linked immunosorbent assay. Results: Most of our patients were males (78.4%) and suffering from lepromatous leprosy (27, 73%) with a mean initial bacillary index of 3.38 ± 1.36. Recurrent and chronic patterns of erythema nodosum leprosum were seen in 15 (40.5%) and 6 (16.3%) patients, respectively. Most (86.5%) of our patients presented with moderate to severe erythema nodosum leprosum. The mean serum macrophage migration inhibitory factor level was 21.86 ± 18.7 ng/ml among patients while it was 11.78 ± 8.4 ng/ml in the control group (P < 0.01). There were no statistically significant correlations of macrophage migration inhibitory factor levels with erythema nodosum leprosum frequency or severity. Limitation: Serum macrophage migration inhibitory factor levels in leprosy patients with no erythema nodosum leprosum and in patients with other inflammatory and autoimmune conditions were not assessed. Hence, this study falls short of providing the predictive value and specificity of higher macrophage migration inhibitory factor concentrations in serum as a biomarker of erythema nodosum leprosum. Conclusion: Macrophage migration inhibitory factor levels are elevated in erythema nodosum leprosum patients as compared to controls. A larger sample size and macrophage migration inhibitory factor gene polymorphism analysis will be needed to elucidate the role of this pro-inflammatory cytokine in erythema nodosum leprosum.
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OBJECTIVE: To observe the effect of electroacupuncture (EA) at "Zusanli" (ST 36) and "Feishu" (BL 13) on pulmonary function, inflammatory reaction and expression of macrophage migration inhibitory factor (MIF) and its receptor complex CD 74-CD 44, etc. in rats with chronic obstructive pulmonary disease (COPD), so as to explore its mechanism underlying improvement of COPD. METHODS: Thirty male SD rats were randomly divided into normal, model and EA groups (n＝10 in each group). The COPD model was established by intratracheal infusion of Lipopolysaccharide (LPS, 1 mg/mL) and forced smoke-inhaling. EA was applied to bilateral ST 36 and BL 13 for 30 min, once daily for 7 days. The rat's lung function (forced vital capacity [FVC], forced expiratory capacity ratio ([FEV 0.1/FVC] and [FEV 0.3/FVC]) was detected under anesthesia. Pathological changes of the lung tissue were detected by H．E. staining, and the contents of MIF, tumor necrosis factor-α (TNF-α), interleukin-1 β (IL-1 β) and IL-8 in serum, bronchoalveolar lavage fluid (BALF) and lung tissue were assayed by ELISA. The immunoactivity of CD 74 and CD 44 was detected by immunohistochemistry, and the expression levels of MIF, CD 74, CD 44 and p 38 MAPK mRNAs and proteins were examined by quantitative RT-PCR and Western blot, respectively. RESULTS: Compared with the normal group, the FVC, FEV 0.1, FEV 0.3, FEV 0.1/FVC and FEV 0.3/FVC levels were significantly decreased in the model group (P<0.01). After EA treatment, the FVC, FEV 0.1, FEV 0.3, FEV 0.1/FVC and FEV 0.3/FVC were significantly increased (P<0.01, P<0.05), suggesting an improvement of the pulmonary function after EA. H．E. staining showed that the severity of modeling induced alveolar expansion and inflammatory cell infiltration in the lung tissue was relatively milder in the EA group relevant to the model group. The contents of MIF, TNF-α， IL-1 β and IL-8 in the serum, BALF and lung tissues were significantly higher in the model group than in the normal group (P<0.01), and significantly down-regulated in the EA group relevant to the model group (P<0.01). The expression levels of MIF, CD 74, CD 44 and p 38 MAPK mRNAs and proteins and the immunoactivity levels of CD 74, CD 44 in the lung tissue were obviously higher in the model group than those in the normal group (P<0.01), and considerably lower in the EA group than those in the model group (P<0.01). There was a positive correlation between p 38 MAPK and MIF in mRNA and protein expression levels (P<0.01). CONCLUSION: EA intervention can improve the pulmonary function in COPD rats, which may be related to its effects in inhibiting inflammatory reaction, and MIF/CD 74-CD 44/p 38 MAPK signaling pathway.
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Objective@#To investigate the association between macrophage migration inhibitory factor (MIF) -173G/C gene polymorphism and the susceptibility to immune-related diseases in Chinese Han population.@*Methods@#Databases of Wanfang, China National Knowledge Infrastructure (CNKI), PubMed, Excerpta Medica dataBASE (EMbase) and Web of Science (WOS) were comprehensively searched for pertinent articles published in Chinese and English. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used as effect size measures. Publication bias was examined by Brgge′s funnel plots and Egger′s test. Revman 5.3 and STATA 12.0 software were used for statistical analysis.@*Results@#Nine articles were included in this meta-analysis and the studied immune-related diseases included UC (ulcerative colitis), CD (Crohn′s disease), RA (rheumatoid arthritis), PS (psoriasis), asthma, BD (Behçet′s disease), VKH (Vogt-Koyanagi-Harada syndrome), AOSD (adult-onset Still′s disease) and AD (atopic dermatitis). The overall result of the meta-analysis showed that the MIF 173G/C gene polymorphism could increase the susceptibility to immune-related diseases in Chinese Han people (recessive genetic model: OR=1.92, 95%CI: 1.44-2.58; dominant genetic model: OR=1.44, 95%CI: 1.28-1.61; allele model: OR=1.34, 95%CI: 1.22-1.34; homozygote model: OR=1.98, 95%CI: 1.51-2.60; heterozygote model: OR=1.24, 95%CI: 1.11-1.40; all P<0.01). In addition, a subgroup analysis of the North and South of China showed that except for the heterozygote model in the North group, the recessive model (OR=2.03, 95%CI: 1.24-3.31), dominant genetic model (OR=1.51, 95%CI: 1.24-1.83), allele model (OR=1.37, 95%CI: 1.22-1.54) and homozygote model (OR=2.08, 95%CI: 1.31-2.30) all had statistical significance. All of the five models in the South group showed statistical significance (recessive model: OR=1.88, 95%CI: 1.31-2.69; dominant genetic model: OR=1.40, 95%CI: 1.22-1.61; allele model: OR=1.29, 95%CI: 1.10-1.52; homozygote model: OR=1.93, 95%CI: 1.38-2.71; heterozygote model: OR=1.19, 95%CI: 1.08-1.31; all P<0.05).@*Conclusion@#The polymorphism of MIF -173G/C gene may be a susceptible gene to immune-related diseases in Chinese Han people.
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Objective To study the effect of macrophage migration inhibitory factor(MIF) antibody on the rat colonic aberrant crypt foci(ACF) induced by 1,2-dimethylhydrazine(DMH),carcinoma number and expression of MIF in rat colonic carcinogenesis.Methods Rat colonic carcinogenesis model was induced by DMH.In this model,the inhibitory effect of MIF antibody on the number of ACF and carcinoma was observed.ELISA and immunohistochemical staining were adopted to investigate the effect of MIF antibody in early cancerative intestinal mucosa and MIF expression after cancer formation.Results The number of ACF and carcinoma was significantly inhibited by MIF antibody intervention(P＜ 0.01).The expression of MIF in the colonic carcinoma model was significantly higher than that in the pre-carcinoma ACF model(P＜0.01).Applying MIF antibody could significantly inhibit the expression of MIF in both rat colonic ACF and colonic carcinoma model.Conclusion MIF antibody can significantly inhibit the rat colonic mucosal carcinogenesis,which may be related with inhibiting number of ACF and expression of MIF.MIF antibody may be expected to become a new target spot of precaution and treatment of colonic carcinoma.
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Macrophage migration inhibitory factor (MIF) is a classical pro-inflammatory cytokine that plays an important role in the innate and adaptive immune regulation. In recent years, a large number of studies have demonstrated that the expression level of MIF is significantly increased in a variety of tumor tissues and MIF promotes the occurrence and development of tumors. MIF participates in the regulation of tumor growth, metastasis, angiogenesis, as well as induces and maintains the tumor microenvironment. Targeting MIF has been considered as a candidate strategy against cancer. In this review, the structural features, the signaling pathway, the biological functions of MIF are briefly outlined. Moreover, approaches that target MIF in the treatment of cancer are also summarized.
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The aim of this study was to investigate the expression of macrophage migration inhibitory factor (MMIF),hypoxia-inducible factor-1 α (HIF-1 αt) and vascular endothelial growth factor (VEGF) in the serum and endometrial tissues of patients with endometriosis (EM) and the clinical significance.Eighty EM patients [American Reproductive Association stage I (n=20),stage Ⅱ (n=22),stage Ⅲ (n=21) and stage Ⅳ (n=17)] were enrolled and divided into mild (10-14 points,n=28),moderate (16-24 points,n=27) and severe (26-30 points,n=25) dysmenorrhea groups.The control group included 40 healthy women of childbearing age who underwent routine healthcare examinations in the enrolment period.The expression of MMIF,HIF-1α and VEGF in the serum and endometrial tissues was measured by enzyme-linked immunosorbent assay and Western blotting,respectively.Meanwhile,the sensitivity and specificity of serum MMIF,HIF-1α,and VEGF when separately used as single indexes or jointly used as one index were examined as well.The results showed that serum concentrations of MMIF,HIF-1α,and VEGF were significantly higher in EM patients than in controls (P＜0.05).The expression of all three proteins in both serum and endometrial tissues increased significantly with the R-AFS stage (P＜0.05) and with dysmenorrheal severity (P＜0.05).The sensitivity and specificity of the combined detection of serum MMIF,HIF-1α,and VEGF levels were significantly higher than those of single index detection (P＜0.05).In conclusion,the expression of MMIF,HIF-1α,and VEGF in the serum and endometrial tissues may be used to assess the stage of EM and the severity of dysmenorrhea.Combined evaluation of MMIF,HIF-1α,and VEGF significantly improves the diagnostic sensitivity and specificity.