Background Mutation or deletion in the phosphatase and tensin homologue deleted on chromosome ten （PTEN） gene has been identified as an important cause of endometrial carcinoma; stromal cell derived factor-1α （SD...Background Mutation or deletion in the phosphatase and tensin homologue deleted on chromosome ten （PTEN） gene has been identified as an important cause of endometrial carcinoma; stromal cell derived factor-1α （SDF-1α） exerts growth-promoting effects on endometrial cancer cells through activation of the PI-3 kinase/Akt pathway and downstream effectors such as extracellular-responsive kinase （ERK）. In this study, a plasmid containing the PTEN gene was transfected into Ishikawa cells to investigate the difference in growth and signal transduction between Ishikawa-PTEN and Ishikawa cells after SDF-1α stimulation, and to study mechanisms of the involvement of PTEN protein in endometrial carcinoma development. Methods Ishikawa cells were transfected with a plasmid （pLXSN-PTEN） containing the PTEN gene and a plasmid （pLXSN-EGFP） with enhanced green fluorescent protein （EGFP）. Cells were then screened to obtain Ishikawa-PTEN cells and Ishikawa-neo cells that can both stably express PTEN protein and EGFP. Expression of PTEN protein, phosphorylation levels of AKT and ERK （pAKT and pERK） and growth differences in Ishikawa-PTEN, Ishikawa-neo and Ishikawa cells before and after SDF-1α stimulation were then determined by Western blots and MTT assays. Results Western blot analysis showed that Ishikawa cells produced PTEN after transfection with the PTEN gene. At 15 minutes after SDF-1α stimulation, the pAKT level of Ishikawa-PTEN cells was lower than that of Ishikawa-neo cells and Ishikawa cells. There was no significant difference in pERK levels among the three cell lines. The positive effect of SDF-1α on Ishikawa-PTEN cells growth was markedly less than the effect on Ishikawa-neo and Ishikawa cells. However, in the absence of SDF-1α stimulation （baseline）, the pAKT level in Ishikawa-PTEN cells was less than that in Ishikawa cells. There was a significant difference in growth between the Ishikawa-PTEN cells and the Ishikawa-neo cells. Conclusions PTEN gene transfection can regulate the le展开更多
目的探讨哮喘小鼠发病过程中基质细胞衍生因子-1(SDF-1)及其受体CXCR4在肺内表达的变化及布地奈德的干预影响。方法清洁级雄性BALB/c小鼠30只,随机分为对照组、干预组及哮喘组。观察卵蛋白激发及用布地奈德干预后哮喘小鼠气道的病理变化...目的探讨哮喘小鼠发病过程中基质细胞衍生因子-1(SDF-1)及其受体CXCR4在肺内表达的变化及布地奈德的干预影响。方法清洁级雄性BALB/c小鼠30只,随机分为对照组、干预组及哮喘组。观察卵蛋白激发及用布地奈德干预后哮喘小鼠气道的病理变化;免疫组织化学染色观察SDF-1表达的变化;RT-PCR法观察CXCR4mRNA表达的变化。结果SDF-1及CXCR4mRNA在对照组中呈低表达,在哮喘组中表达明显增加,使用布地奈德进行干预后SDF-1及CXCR4 mRNA的表达明显降低(0.426±0.052 vs 0.361±0.065;0.829±0.027 vs 0.723±0.094;P<0.05),且二者表达量均与气道壁厚度呈正相关(r=0.744,P<0.01;r=0.553,P<0.01)。结论SDF-1及其受体CXCR4可能参与了哮喘小鼠气道重塑过程,布地奈德干预改善哮喘小鼠的气道重塑可能与降低SDF-1及CXCR的表达有关。展开更多
目的:观察子宫内膜异位症大鼠异位内膜组织基质细胞衍生因子-1(SDF-1)及其趋化因子受体(CXCR4)的表达情况,并探讨复方莪术散对其表达的影响。方法:自体移植法建立非动情期SD大鼠子宫内膜异位症模型,PCR法检测大鼠在位、异位内膜组织及...目的:观察子宫内膜异位症大鼠异位内膜组织基质细胞衍生因子-1(SDF-1)及其趋化因子受体(CXCR4)的表达情况,并探讨复方莪术散对其表达的影响。方法:自体移植法建立非动情期SD大鼠子宫内膜异位症模型,PCR法检测大鼠在位、异位内膜组织及正常在位子宫内膜组织SDF-1和CXCR4的m RNA表达,分析各组统计学差异;造模21 d后,分组连续给药28 d,对比观察中药复方莪术散(高、中、低剂量组各10只)与模型组(10只)异位症内膜组织中SDF-1 m RNA,CXCR4 m RNA的表达差异。结果:SDF-1 m RNA和CXCR4 m RNA在大鼠异位内膜组织高表达,与在位内膜组织及正常子宫内膜组织比较有统计学差异(P<0.05);各治疗组异位内膜组织SDF-1m RNA表达均下降,高剂量组(0.646±0.264)与中、低剂量组(1.001±0.160、1.714±0.343)比较降低明显,且各组间比较有统计学意义(P<0.05);各治疗组CXCR4 m RNA表达有下降趋势,复方莪术散高剂量(0.587±0.476)和复方莪术散中剂量(1.408±0.252)组CXCR4 m RNA表达分别与模型组(3.004±0.264)比较有统计学差异(P<0.05)。结论:SDF-1、CXCR4在大鼠在位内膜组织中的表达高于正常子宫内膜组织,其表达可能与大鼠子宫内膜异位症的发病机制存在一定关系。复方莪术散可明显降低异位内膜组织中SDF-1、CXCR4表达,对子宫内膜异位症有一定治疗作用。展开更多
基金This work was supported by a grant from the National Natural Science Foundation of China (No.30571938).
文摘Background Mutation or deletion in the phosphatase and tensin homologue deleted on chromosome ten （PTEN） gene has been identified as an important cause of endometrial carcinoma; stromal cell derived factor-1α （SDF-1α） exerts growth-promoting effects on endometrial cancer cells through activation of the PI-3 kinase/Akt pathway and downstream effectors such as extracellular-responsive kinase （ERK）. In this study, a plasmid containing the PTEN gene was transfected into Ishikawa cells to investigate the difference in growth and signal transduction between Ishikawa-PTEN and Ishikawa cells after SDF-1α stimulation, and to study mechanisms of the involvement of PTEN protein in endometrial carcinoma development. Methods Ishikawa cells were transfected with a plasmid （pLXSN-PTEN） containing the PTEN gene and a plasmid （pLXSN-EGFP） with enhanced green fluorescent protein （EGFP）. Cells were then screened to obtain Ishikawa-PTEN cells and Ishikawa-neo cells that can both stably express PTEN protein and EGFP. Expression of PTEN protein, phosphorylation levels of AKT and ERK （pAKT and pERK） and growth differences in Ishikawa-PTEN, Ishikawa-neo and Ishikawa cells before and after SDF-1α stimulation were then determined by Western blots and MTT assays. Results Western blot analysis showed that Ishikawa cells produced PTEN after transfection with the PTEN gene. At 15 minutes after SDF-1α stimulation, the pAKT level of Ishikawa-PTEN cells was lower than that of Ishikawa-neo cells and Ishikawa cells. There was no significant difference in pERK levels among the three cell lines. The positive effect of SDF-1α on Ishikawa-PTEN cells growth was markedly less than the effect on Ishikawa-neo and Ishikawa cells. However, in the absence of SDF-1α stimulation （baseline）, the pAKT level in Ishikawa-PTEN cells was less than that in Ishikawa cells. There was a significant difference in growth between the Ishikawa-PTEN cells and the Ishikawa-neo cells. Conclusions PTEN gene transfection can regulate the le
文摘目的探讨哮喘小鼠发病过程中基质细胞衍生因子-1(SDF-1)及其受体CXCR4在肺内表达的变化及布地奈德的干预影响。方法清洁级雄性BALB/c小鼠30只,随机分为对照组、干预组及哮喘组。观察卵蛋白激发及用布地奈德干预后哮喘小鼠气道的病理变化;免疫组织化学染色观察SDF-1表达的变化;RT-PCR法观察CXCR4mRNA表达的变化。结果SDF-1及CXCR4mRNA在对照组中呈低表达,在哮喘组中表达明显增加,使用布地奈德进行干预后SDF-1及CXCR4 mRNA的表达明显降低(0.426±0.052 vs 0.361±0.065;0.829±0.027 vs 0.723±0.094;P<0.05),且二者表达量均与气道壁厚度呈正相关(r=0.744,P<0.01;r=0.553,P<0.01)。结论SDF-1及其受体CXCR4可能参与了哮喘小鼠气道重塑过程,布地奈德干预改善哮喘小鼠的气道重塑可能与降低SDF-1及CXCR的表达有关。
文摘目的:观察子宫内膜异位症大鼠异位内膜组织基质细胞衍生因子-1(SDF-1)及其趋化因子受体(CXCR4)的表达情况,并探讨复方莪术散对其表达的影响。方法:自体移植法建立非动情期SD大鼠子宫内膜异位症模型,PCR法检测大鼠在位、异位内膜组织及正常在位子宫内膜组织SDF-1和CXCR4的m RNA表达,分析各组统计学差异;造模21 d后,分组连续给药28 d,对比观察中药复方莪术散(高、中、低剂量组各10只)与模型组(10只)异位症内膜组织中SDF-1 m RNA,CXCR4 m RNA的表达差异。结果:SDF-1 m RNA和CXCR4 m RNA在大鼠异位内膜组织高表达,与在位内膜组织及正常子宫内膜组织比较有统计学差异(P<0.05);各治疗组异位内膜组织SDF-1m RNA表达均下降,高剂量组(0.646±0.264)与中、低剂量组(1.001±0.160、1.714±0.343)比较降低明显,且各组间比较有统计学意义(P<0.05);各治疗组CXCR4 m RNA表达有下降趋势,复方莪术散高剂量(0.587±0.476)和复方莪术散中剂量(1.408±0.252)组CXCR4 m RNA表达分别与模型组(3.004±0.264)比较有统计学差异(P<0.05)。结论:SDF-1、CXCR4在大鼠在位内膜组织中的表达高于正常子宫内膜组织,其表达可能与大鼠子宫内膜异位症的发病机制存在一定关系。复方莪术散可明显降低异位内膜组织中SDF-1、CXCR4表达,对子宫内膜异位症有一定治疗作用。
