To summarize Notch, basic hel ix-loop-hel ix (bHLH) and Wnt gene signal transduction pathways in the process of differentiation and development of neural stem cells. Methods The l iterature on the gene signal transduction pathway in the process of differentiation and development of neural stem cells was searched and then summarized and analyzed. Results The formation of Nervous System resulted from common actions of multi-signal transduction pathways. There may exist a fixed threshold in the compl icated selective system among Notch, bHLH and Wnt gene signal transduction pathways. Conclusion At present, the specific gene signal transduction pathway of multi pl ication and differentiation of neural stem cells is still unclear.
目的 研究活动期多发性肌炎患者外周血白细胞细胞因子信号转导蛋白抑制因子（SOCS）1、SOCS2、SOCS3和细胞因子诱导的含SH2区域蛋白1（CIS）与正常人表达的差异，探讨SOCS在多发性肌炎发病中可能的作用。 方法 2011年6月－12月，采用实时荧光定量聚合酶链反应法检测了14例活动期多发性肌炎患者和14例正常人外周血白细胞中SOCS1、SOCS2、SOCS3和CIS1基因的相对表达量。 结果 与对照组相比，多发性肌炎症患者外周血白细胞基因SOCS 1～3表达明显降低（P值均＜0.05），CIS1基因的表达较对照组明显升高（P＜0.05），差异有统计学意义。 结论 SOCS基因家族可能参与了多发性肌炎的发病，该蛋白分子家族的成员可能会成为多发性肌炎治疗的一种新的候选基因。
Objective To construct AWP1 (associated with protein kinase C related kinase 1) recombinant adenovirus as the tool of transferring the gene and investigate its expression and localization in human vascular endothelial cell ECV304. Methods Cloned AWP1 cDNA was inserted into the multiply clone sites (MCS) of plasmid pcDNA3 for adding flag tag, and the flag-AWP1 gene was subcloned into shuttle vector pAdTrack-CMV. After identified with restrictional enzymes, plasmid pAdTrack-flag-AWP1 was linearized by digestion with restriction endonuclease PmeⅠ, and subsequently cotransformed into E.coli BJ5183 cells with adenoviral backbone plasmid pAdEasy-1 to make homologous recombination. After linearized by PacⅠ, the homologous recombinant adenovirus plasmid transfected into 293 cells with Lipofectamine to pack recombinant adenovirus. After PCR assay of recombinant adenovirus granules, recombinant adenoviruses infected 293 cells repeatedly for obtaining the high-level adenoviruses solution. And then, the recombinant adenoviruses infected human ECV304 cells for observing the expression and localization of AWP1 under laser scanning confocal microscope (LSCM). Results PCR assay showed that recombinant adenovirus Ad-flag-AWP1 was obtained successfully; and ECV304 cells were infected high-efficiently by the homologous recombinant virus. Then, it was observed that flag-AWP1 protein expressed in ECV304 cells and distributed in the leading edges of the cell membrane. Conclusion The vectors of flag-AWP1 recombinant adenovirus are constructed, and the localization of AWP1 protein in ECV304 cells might show that AWP1 may be a potential role on the cell signal transduction.
ObjectiveTo investigate the expressions of Patched-1 (Ptch1) and glioma-associated oncogene homologl (Gli1) protein of sonic hedgehog signaling pathway in cholangiocarcinoma tissues, and explore their correlations to the occurrence and development of cholangiocarcinoma. MethodsThe expressions of Ptch1 and Gli1 protein in 62 specimens of cholangiocarcinoma and its bile duct tissues adjacent to cancer were detected by immunohistochemistry, and their positive rate correlated with patients, age, tumor size, differentiation grade, tumor location, lymph node metastasis, TNM stage, operation mode, and postoperative survival time were investigated by statistical analysis. ResultsThe positive rates of Ptch1 and Gli1 protein were significantly higher in cholangiocarcinoma than in tissues adjacent to cancer (74.2% vs. 14.5%, 88.7% vs. 9.7%, P < 0.05). The expressions of Ptch1 and Gli1 protein in cholangiocarcinoma had no correlation to patients age, tumor size, and tumor location (P > 0.05), but were correlated to the operation mode, differentiation grade, lymph node metastasis, TNM stage, and postoperative survival time of patients (P < 0.05). ConclusionsThe elevated expressions of Ptch1 and Gli1 protein of Hh signaling pathway participated in the occurrence and development of cholangiocarcinoma. They may be ideal targets for therapy against cholangiocarcinoma.
Rheumatoid arthritis (RA) is a chronic autoimmune disease remarkably characterized by synovitis of joints, whose pathogenesis is complicated and not yet fully elucidated. A variety of cells, cytokines and intercellular signaling pathways are involved in the occurrence and development of RA. The mitogen activation protein kinase (MAPK) signaling pathway is closely related to the pathogenesis of RA, and plays an important role in the formation of pannus, synovitis, and bone destruction. This paper reviews the research progress of MAPK signaling pathway in RA from the aspects of the interaction of MAPK signaling pathway with a variety of key cells and cytokines in the pathogenesis of RA, in order to provide a direction and theoretical basis for anti-RA drug therapy research.
Objective To study the leptin-mediated intracellular signal pathways and their effects on wound healing.Methods The literature was reviewed extensively, concerning the physical and chemical characters of leptin, the mechanism of its receptor action, the receptor-related intracellular signal pathways and their roles on wound healing. Results Leptin was a protein hormone expressed by ob gene with relative molecular mass 16×103, it could activate the main singal pathways such as Janus kinase/signal transducer and activator of transcription, mitogenactivated protein kinases and phosphoinositide-3-kinase pathways through binding with its specific receptor, to participate in the modulation of multiple functions including energy metabolism, weight balance and wound healing. Leptin receptors were widely distributed in various tissues, which suggest the multiple functions of leptin. Local leptin expression was increased after skin injured, and it could stimulate keratinocytes proliferation, epithelialization, fibroblast proliferation and collagen synthesis, resulting in accelarated wound repair. Leptin expression was significantly increased after mucosal injury or bacteria infections, leading to accelarated mucosal repair through modulation of mucosal glandular secretion, improvment of mucosal blood flow, and synergistic action with endothelin-1.Conclusion Leptin can promote wound healing through activating its receptor-related intracellular signal pathways.
目的 研究活动期多发性肌炎患者外周血白细胞细胞因子信号转导蛋白抑制因子（SOCS）1、SOCS2、SOCS3和细胞因子诱导的含SH2区域蛋白1（CIS）与正常人表达的差异，探讨SOCS在多发性肌炎发病中可能的作用。 方法 2011年6月－12月，采用实时荧光定量聚合酶链反应法检测了14例活动期多发性肌炎患者和14例正常人外周血白细胞中SOCS1、SOCS2、SOCS3和CIS1基因的相对表达量。 结果 与对照组相比，多发性肌炎症患者外周血白细胞基因SOCS 1～3表达明显降低（P值均＜0.05），CIS1基因的表达较对照组明显升高（P＜0.05），差异有统计学意义。 结论 SOCS基因家族可能参与了多发性肌炎的发病，该蛋白分子家族的成员可能会成为多发性肌炎治疗的一种新的候选基因。
ObjectiveTo investigate the expression of interleukin-18（IL-18）and signal transducers and activators of transcription 5（STAT5）in retina of 4-24-week-old diabetic rats, and explore the potential molecular mechanisms involved in diabetic retinopathy (DR).MethodsRetinal gene expression profile of healthy and 8-week-old diabetic rats was established with restriction fragment differential displaypolymerase chained reaction (RFDD-PCR), and the differences was analyzed by bioinformatics. IL-18 and STAT5 were filtrated as the candidate genes of DR. The expression of IL-18 and STAT5 in retina of diabetic rats with the age of 4, 8, and 24 weeks was observed by semi-quantitative reverse transcriptase-polymerase chain reaction（RT-PCR）.ResultsThe result of RFDD-PCR showed:expression of IL-18 was higher in healthy retina than that in diabetic one; expression of STAT5 was not found in healthy rats but in diabetic ones. The result of RT-PCR showed：compared with the normal, high expression of IL-18 was found in 4-week diabetic retina, reduced in 8-week one, and decreased to the lowest in 24-week one. The expression of STAT5 was not observed in healthy or 4week diabetic retina, but occurred in 8-week one, and increased in 24-week one. ConclusionThe expression of IL-18 and the activation of STAT5 may relate to the occurrance of DR. The expression of IL-18 doesn′t depend on the activation of STAT5. (Chin J Ocul Fundus Dis, 2005,21:258-260)
ObjectiveTo investigate the effect of icaritin on the small cell lung cancer cell lines NCI-H446 and its mechanism. MethodsThe NCI-H446 cells at logarithmic growth phase were divided into control and icaritin groups. The cells in the control group were normally treated and cells in the icaritin group were incubated with icaritin (8 μmol/L). Thiazole blue and flow cytometry were used to examine the proliferation and apoptotic changes in the two groups 48 hours after incubation respectively. Gene expression of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3) were detected by real-time quantitative polymerase chain reaction. The changes of JAK2, STAT3, phospho-JAK2 (p-JAK2), phospho-STAT3 (p-STAT3), Bax and BCL-2 protein were detected by Western blotting. ResultsCompared with the control group, the proliferation rate of NCI-H446 cells in the icaritin group was significantly lower (P<0.05), but the apoptotic rate of NCI-H446 cells in the icaritin group was significantly higher (P<0.05). After the treatment with icaritin, the expression of JAK2 and STAT3 mRNA had no obvious differences. The Western blotting results showed that there was no significant changes in total JAK2, STAT3 protein (P>0.05), but an increasing trend in p-JAK2, p-STAT3 and Bax was observed with the decreasing of BCL-2 (P<0.05). ConclusionIcaritin can inhibit the proliferation and promote the apoptosis of NCI-H446 cells and the effect may be achieved through JAK2/STAT3 signal transduction pathway.