The JAR choriocarcinoma cell line share many of the characteristics of early placental trophoblast cells including the invasion properties. Matrix metallo-proteinases (MMPs), the main actors of matrix proteolysis, are...The JAR choriocarcinoma cell line share many of the characteristics of early placental trophoblast cells including the invasion properties. Matrix metallo-proteinases (MMPs), the main actors of matrix proteolysis, are involved in normal invasion as well as in the invasive character of tumor cells and the metastase formation. Tumor necrosis factor-α (TNF-α) is present in the placental environment and TNF-α levels are elevated in some placental pathologies. In the present work, we addressed whether TNF-α is a modulator of JAR cell MMP secretion. Following TNF-α stimulation, zymographic analysis showed the increased secretion of the active form of MMP-2 and to a lesser extent proMMP-2 and MMP-9. In addition, MMP-2 gene expression only increased slightly whereas MMP-9 and TIMP-1 transcripts were undetectable. This suggests that TNF-α may modulate the secretion of MMPs independently of MMP gene expression control.展开更多
摘要目的：观察和分析冠心病患者中肿瘤坏死因子-α诱导蛋白-8样分子．2（tumornecrosisfactor．dinduced protein 8 like2，TIPE2）表达水平及其与单核细胞趋化因子-1（MCP-1）和基质金属蛋白酶-9（MMP-9）的相关性。方法：2010年12月-...摘要目的：观察和分析冠心病患者中肿瘤坏死因子-α诱导蛋白-8样分子．2（tumornecrosisfactor．dinduced protein 8 like2，TIPE2）表达水平及其与单核细胞趋化因子-1（MCP-1）和基质金属蛋白酶-9（MMP-9）的相关性。方法：2010年12月-2012年11月在我院行冠脉造影检查确诊冠心病患者100例，并根据冠脉病变的支数分组，并人选同时期在我院行冠脉造影术明确无冠脉狭窄的非冠心病组（30例）。采用聚合酶链式反应（PCR）测定外周血单个核细胞中TIPE2的基因水平，采用双抗体夹心ELISA法测定血清中MCP-1和MMP-9水平。结果：①外周血单个核细胞TIPE2基因表达水平测定的结果：冠脉病变患者PBMC中TIPE2的基因表达水平明显低于非冠心病组，双支病变组低于单支病变组，多支病变组明显低于单支病变组和双支病变组，差异均具有统计学意义（P〈0．01）；②TIPE2基因表达水平与MCP-1、MMP-9水平呈负相关，相关系数分别为r=-0．560，r=-0．569，均P〈0．05）。结论：冠心病患者中TIPE2表达水平随冠脉病变血管支数的增加而降低，而且与MCP-1和MMP-9呈负相关。展开更多
Background:Henoch-Schönlein purpura(HSP)or IgAassociated vasculitis is related to immune disturbances.Polymorphisms of the heat shock protein 70-2 gene(HSP70-2)and the tumor necrosis factor-αgene(TNF-α)are know...Background:Henoch-Schönlein purpura(HSP)or IgAassociated vasculitis is related to immune disturbances.Polymorphisms of the heat shock protein 70-2 gene(HSP70-2)and the tumor necrosis factor-αgene(TNF-α)are known to be associated with immune diseases.The purpose of this study was to investigate the likely association of HSP70-2(+1267A/G)and TNF-α(+308A/G)gene polymorphisms with HSP in children.Methods:The polymerase chain reaction restriction fragment length polymorphism method was used to detect the HSP70-2 and TNF-αpolymorphisms in 205 cases of children with HSP and 53 controls;and the association of these polymorphisms with HSP and HSP nephritis(HSPN)was analyzed.Results:The G/G genotypic frequencies at the+1267A/G position of HSP70-2 in the HSP group(22.9%)were signifi cantly higher than those in the healthy control group(9.4%)(χ^(2)=4.764,P<0.05).The frequencies of the A/A,A/G and G/G genotypes of HSP70-2 in patients in the nephritis-free group and the HSPN group showed no statistically significant difference.The A/A genotype frequency at the+308G/A position of TNF-αin the HSP group was 8.3%,which was higher than that in the control group(χ^(2)=6.447,P<0.05).The A allele frequency of TNF-αin the HSP group was higher than that in the control group,with a statistically significant difference(χ^(2)=7.241,P<0.05).Conclusions:The HSP70-2(+1267A/G)and TNF-α(+308G/A)gene polymorphisms were associated with HSP in children.The G/G homozygosity of HSP70-2 and the A/A homozygosity of TNF-αmay be genetic predisposing factors for HSP.展开更多
Purpose: Bursal inflammation is thought to be a major cause of pain in degenerative rotator cuff tears (RCTs). While the expression of proinflammatory mediators, such as COX-2, TNF-α, IL-1β, and IL-6, is crucial for...Purpose: Bursal inflammation is thought to be a major cause of pain in degenerative rotator cuff tears (RCTs). While the expression of proinflammatory mediators, such as COX-2, TNF-α, IL-1β, and IL-6, is crucial for the pathophysiology of osteoarthritis (OA), their role in degenerative RCTs remains unknown. The aim of this study was to determine the expression of COX-2 and proinflammatory mediators in the development of RCT-induced pain by comparing their levels in patients with hip OA or RCTs. Methods: We included samples obtained from 31 shoulders of 31 patients with RCTs and samples from 30 hips of 27 patients with hip OA. The mRNA levels of COX-2, TNF-α, IL-1β, and IL-6 were determined using RT-PCR, and were compared between the subacromial bursa and hip joints. We also analyzed IL-1β-induced COX-2 expression in the subacromial bursa and synovial blast of the hip. Results: COX-2, IL-1β, and IL-6 expression levels were significantly lower in the subacromial bursa of RCTs than in hip OA samples, while no significant difference was observed for TNF-α. No significant difference in the fold increase was observed between subacromial bursa and hip OA samples, even though IL-1β-induced COX-2 expression increased in both samples. Conclusion: Our findings suggest that the main mechanism underlying pain development differs between patients with RCTs and those with hip OA.展开更多
基金supported by a grant from the French National League against Cancer,Committee of the Marne.
文摘The JAR choriocarcinoma cell line share many of the characteristics of early placental trophoblast cells including the invasion properties. Matrix metallo-proteinases (MMPs), the main actors of matrix proteolysis, are involved in normal invasion as well as in the invasive character of tumor cells and the metastase formation. Tumor necrosis factor-α (TNF-α) is present in the placental environment and TNF-α levels are elevated in some placental pathologies. In the present work, we addressed whether TNF-α is a modulator of JAR cell MMP secretion. Following TNF-α stimulation, zymographic analysis showed the increased secretion of the active form of MMP-2 and to a lesser extent proMMP-2 and MMP-9. In addition, MMP-2 gene expression only increased slightly whereas MMP-9 and TIMP-1 transcripts were undetectable. This suggests that TNF-α may modulate the secretion of MMPs independently of MMP gene expression control.
文摘摘要目的：观察和分析冠心病患者中肿瘤坏死因子-α诱导蛋白-8样分子．2（tumornecrosisfactor．dinduced protein 8 like2，TIPE2）表达水平及其与单核细胞趋化因子-1（MCP-1）和基质金属蛋白酶-9（MMP-9）的相关性。方法：2010年12月-2012年11月在我院行冠脉造影检查确诊冠心病患者100例，并根据冠脉病变的支数分组，并人选同时期在我院行冠脉造影术明确无冠脉狭窄的非冠心病组（30例）。采用聚合酶链式反应（PCR）测定外周血单个核细胞中TIPE2的基因水平，采用双抗体夹心ELISA法测定血清中MCP-1和MMP-9水平。结果：①外周血单个核细胞TIPE2基因表达水平测定的结果：冠脉病变患者PBMC中TIPE2的基因表达水平明显低于非冠心病组，双支病变组低于单支病变组，多支病变组明显低于单支病变组和双支病变组，差异均具有统计学意义（P〈0．01）；②TIPE2基因表达水平与MCP-1、MMP-9水平呈负相关，相关系数分别为r=-0．560，r=-0．569，均P〈0．05）。结论：冠心病患者中TIPE2表达水平随冠脉病变血管支数的增加而降低，而且与MCP-1和MMP-9呈负相关。
基金supported by grants from the National Natural Science Foundation of China(No.81170635,81270785).
文摘Background:Henoch-Schönlein purpura(HSP)or IgAassociated vasculitis is related to immune disturbances.Polymorphisms of the heat shock protein 70-2 gene(HSP70-2)and the tumor necrosis factor-αgene(TNF-α)are known to be associated with immune diseases.The purpose of this study was to investigate the likely association of HSP70-2(+1267A/G)and TNF-α(+308A/G)gene polymorphisms with HSP in children.Methods:The polymerase chain reaction restriction fragment length polymorphism method was used to detect the HSP70-2 and TNF-αpolymorphisms in 205 cases of children with HSP and 53 controls;and the association of these polymorphisms with HSP and HSP nephritis(HSPN)was analyzed.Results:The G/G genotypic frequencies at the+1267A/G position of HSP70-2 in the HSP group(22.9%)were signifi cantly higher than those in the healthy control group(9.4%)(χ^(2)=4.764,P<0.05).The frequencies of the A/A,A/G and G/G genotypes of HSP70-2 in patients in the nephritis-free group and the HSPN group showed no statistically significant difference.The A/A genotype frequency at the+308G/A position of TNF-αin the HSP group was 8.3%,which was higher than that in the control group(χ^(2)=6.447,P<0.05).The A allele frequency of TNF-αin the HSP group was higher than that in the control group,with a statistically significant difference(χ^(2)=7.241,P<0.05).Conclusions:The HSP70-2(+1267A/G)and TNF-α(+308G/A)gene polymorphisms were associated with HSP in children.The G/G homozygosity of HSP70-2 and the A/A homozygosity of TNF-αmay be genetic predisposing factors for HSP.
文摘Purpose: Bursal inflammation is thought to be a major cause of pain in degenerative rotator cuff tears (RCTs). While the expression of proinflammatory mediators, such as COX-2, TNF-α, IL-1β, and IL-6, is crucial for the pathophysiology of osteoarthritis (OA), their role in degenerative RCTs remains unknown. The aim of this study was to determine the expression of COX-2 and proinflammatory mediators in the development of RCT-induced pain by comparing their levels in patients with hip OA or RCTs. Methods: We included samples obtained from 31 shoulders of 31 patients with RCTs and samples from 30 hips of 27 patients with hip OA. The mRNA levels of COX-2, TNF-α, IL-1β, and IL-6 were determined using RT-PCR, and were compared between the subacromial bursa and hip joints. We also analyzed IL-1β-induced COX-2 expression in the subacromial bursa and synovial blast of the hip. Results: COX-2, IL-1β, and IL-6 expression levels were significantly lower in the subacromial bursa of RCTs than in hip OA samples, while no significant difference was observed for TNF-α. No significant difference in the fold increase was observed between subacromial bursa and hip OA samples, even though IL-1β-induced COX-2 expression increased in both samples. Conclusion: Our findings suggest that the main mechanism underlying pain development differs between patients with RCTs and those with hip OA.
