摘要：
Aim: This study was conducted to reveal new proteins involved in acute myeloid leukemia (AML) cell apoptosis. Methods: Using camptothecin analog NSC606985-induced leukemic U937 cell apoptosis as a model, this study performed a differential proteomic analysis during apoptosis induction. The significantly modulated protein was underwent further investigation in the apoptotic process. Results: We found that β-actin protein presented two different spots on the two-dimensional electrophoresis (2-DE) map, which shared similar molecular weight and different pI. Those two spots demonstrated contrary changes (disappeared on the basic-end and increased on the acid-end spot) during apoptosis induction, although the total level of β-actin kept constant. This observation was further confirmed by immunoblot analysis on 2-DE gel. When NSC606985-treated cell lysate was incubated with alkaline phosphotase, β-actin on the basic-end spot was restored, indicating increased phosphorylation of β-actin during NSC606985-induced apoptosis. Moreover, the polymerization of actin also decreased after NSC606985 treatment. The increased β-actin phosphorylation and decreased actin polymerization was antagonized by pre-treatment of rottlerin, a specific protein kinase C-delta (PKCδ) inhibitor. Conclusion: All these results indicate that β-actin was phosphorylated during apoptosis induction, which was mediated by activated PKCδ.
摘要：
Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Vascular smooth muscle cells express both apelin and APJ, which are important regulatory factors in the cardiovascular and nervous systems. Importantly, APJ is also involved in the pathogenesis if HIV-1 infection. We investigated whether vascular smooth muscle cell proliferation was regulated through an apelin-pERK1/2-cyclin D1 signal transduction pathway. Apelin-13 significantly stimulated vascular smooth muscle cell proliferation and increased cell cycle progression. Apelin-13 a decreased the proportion of cell in the G0/G1 phase while increasing the number of cells in S phase. Apelin-13 also increased the levels of cyclin D1, cyclin E and pERK1/2. Treatment of cells with the MEK inhibitor PD98059 attenuated the apelin-3-induced pERK1/2 activation. Similarly, treatment with PD98059 partially diminished the apelin-13-induced expression of cyclin D1 and vascular smooth muscle cell proliferation. Taken together, these data established that apelin-13 stimulates vascular smooth muscle cell proliferation by promoting the G1-S phase transition, and that this effect is mediated in part by an apelin-pERKl/2-cyclin D1 signal cascade.
通讯机构：
[Li, Shuangjie] U;Univ S China, Hosp 1, Dept Paediat, 69 Chuan Shan Rd, Hengyang 421001, Hunan, Peoples R China.
关键词：
stem cell;viral myocarditis;proliferation
摘要：
Our goal was to investigate temporal changes in stem cell in the circulation and myocardium of mice with Coxsackie virus B3-induced myocarditis. Groups of mice were administered Eagle's minimal essential medium or virus solution. The animals were further divided into six subgroups based on the following time points post-inoculation: 1, 3, 7, 14, 21, and 28 days. Ten animals were studied in each subgroup. Circulating blood mononuclear cells were collected from the heart and analyzed using flow cytometry. Myocardial inflammation, stem cell expression, and cell proliferation were detected by histology and immunofluorescence. H&E staining revealed neutrophil infiltration and bleeding by day 3 post-infection. Myeloperoxidase and reactive oxygen species levels peaked by day 3 and were followed by myocyte loss and collagen deposition. Circulating mesenchymal stem cells also peaked by day 3. In contrast, hematopoietic stem cells remained sustained increase within day 14. Immunohistochemical microscopy also showed a marked increase in cardiac stem cells by day 14. The kinetics of this increase was consistent with a rise in proliferating cells expressing nuclear and cytoplasmic proteins that are typical of cardiomyocyte or vascular endothelial cells. These results demonstrate the rapid kinetics of progenitor cells during viral myocarditis and suggest that the optimal time to administer cell therapy to induce heart repair is within 2 weeks after viral infection.
作者机构：
[Chen Lin; Yu Min-jun; Wan Yan-ping; Zhu Cui-ming; Cao Qing-xiang; Liu An-yuan; Chan Xi] Univ S China, Inst Pathogen Biol, Hengyang 421001, Peoples R China.
通讯机构：
[Wan Yan-ping] U;Univ S China, Inst Pathogen Biol, Hengyang 421001, Peoples R China.
关键词：
human cytomegalovirus ( HCMV);IE1;macrophages;IL-1 beta;TNF-alpha;apoptosis
摘要：
Objective: To investigate the effect of human cytomegalovirus (HCMV) IE1 protein on the secretory activity and apoptosis of macrophages. Methods: The eukaryotic expression vector pEGFP-C1/IE1 was used to transfect THP-1-macrophages. 48 h after transfection, the expression and localization of GFP or GFP-IE1 was observed under fluorescent microscope. The levels of IL-1β and TNF-α in the culture media were examined by ELISA, and the mRNA expression of them was analyzed by RT-PCR. Cell undergoing apoptosis were determined by flow cytometry using the propidium iodide (PI) staining method. The data were analyzed by SPSS 13.0. Results: As observed under fluorescent microscope, the expressions of GFP-IE1 and GFP by plasmid pEGFP-C1/IE1 or pEGFP-C1 in THP-1-macrophages could be found in nuclei or whole cells. Conclusion: As demonstrated by RT-PCR and ELISA, mRNA and protein expressions of IL-1β and TNF-α and promotes apoptosis in THP-1-macrophages.
摘要：
The pathogenesis of nasopharyngeal carcinoma (NPC) is a complicated process involving genetic predisposition, Epstein-Bar Virus infection, and genetic alterations. Although some oncogenes and tumor suppressor genes have been previously reported in NPC, a complete understanding of the pathogenesis of NPC in the context of global gene expression, transcriptional pathways and biomarker assessment remains to be elucidated. Total RNA from 32 pathologically-confirmed cases of poorly-differentiated NPC was divided into pools inclusive of four consecutive specimens and each pool (T1 to T8) was co-hybridized with pooled RNA from 24 normal non-cancerous nasopharyngeal tissues (NP) to a human 8K cDNA array platform. The reliability of microarray data was validated for selected genes by semi-quantitative RT-PCR and immunohistochemistry. Stringent statistical filtering parameters identified 435 genes to be up-regulated and 257 genes to be down-regulated in NPC compared to NP. Seven up-regulated genes including CYC1, MIF, LAMB3, TUBB2, UBE2C and TRAP1 had been previously proposed as candidate common cancer biomarkers based on a previous extensive comparison among various cancers and normal tissues which did not, however, include NPC or NP. In addition, nine known oncogenes and tumor suppressor genes, MIF, BIRC5, PTTG1, ATM, FOXO1A, TGFBR2, PRKAR1A, KLF5 and PDCD4 were identified through the microarray literature-based annotation search engine MILANO, suggesting these genes may be specifically involved in the promotion of the malignant conversion of nasopharyngeal epithelium. Finally, we found that these differentially expressed genes were involved in apoptosis, MAPK, VEGF and B cell receptor signaling pathways and other functions associated with cell growth, signal transduction and immune system activation. This study identified potential candidate biomarkers, oncogenes/tumor suppressor genes involved in several pathways relevant to the oncogenesis of NPC. This information may facilitate the determination of diagnostic and therapeutic targets for NPC as well as provide insights about the molecular pathogenesis of NPC.
摘要：
Previous studies demonstrated the EGF-targeted phagemid particles carrying siRNA against Akt could be expressed efficiently in the presence of hydroxycamptothecin (HCPT). However, no significant cell growth inhibition was obtained. This study was to further investigate whether the EGF-targeted phagemid particles carrying siRNA would be a promising tool for anti-cancer siRNA delivery. We found that pSi4.1-siFAK phagemid particles could significantly inhibit the expression of focal adhesion kinase in the HCPT-treated cells. Moreover, we also observed that the particles could potently suppress cell growth and cell invasion. These results indicated that EGF-targeted phagemid particles might be a promising tool for anti-cancer siRNA delivery in the presence of HCPT.
摘要：
5-Fluorouracil (5-FU) is an important chemotherapeutic agent for nasopharyngeal carcinoma (NPC). However, drug resistance may occur after several cycles of 5-FU-based chemotherapy. The oncogene B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI-1) has been shown to be involved in the protection of cancer cells from apoptosis. In this study, 5-FU treatment could increase the percentage of apoptotic NPC cells among BMI-1/RNAi-transfected cells than that among cells transfected with the empty vector. The 50% inhibitory concentration (IC(50)) values of 5-FU were significantly decreased to a greater extent in the cells transfected with BMI-1/RNAi. Most importantly, the expression of phospho-Ala and the anti-apoptotic protein BCL-2 were downregulated in the cells in which BMI-1 expression was inhibited, whereas the apoptosis-inducer BAX was observed to be upregulated. Abrogation of AI(T pathway by a PI3K inhibitor could not further increase the sensitivity to 5-FU in the cells with reduced BMI-1 expression. Taken together, BMI-1 depletion enhanced the chemosensitivity of NPC cells by inducing apoptosis; which is associated with inhibition of the PI3K/AKT pathway. (C) 2008 Elsevier Inc. All rights reserved.
期刊：
SCIENCE IN CHINA SERIES A-MATHEMATICS,2008年51(8):1537-1548 ISSN：1006-9283
通讯作者：
Shu Shi
作者机构：
[Shu Shi; Zhong LiuQiang] Xiangtan Univ, Sch Math & Computat Sci, Xiangtan 411105, Peoples R China.;[Shu Shi; Zhong LiuQiang] Hunan Key Lab Computat & Simulat Sci & Engn, Xiangtan 411105, Peoples R China.;[Sun Dudu] Chinese Acad Sci, Grad Univ, Acad Math & Syst Sci, Inst Computat Math & Sci Engn Comp, Beijing 100190, Peoples R China.;[Tan Lin] Nanhua Univ, Dept Math Phys, Hengyang 421001, Peoples R China.
通讯机构：
[Shu Shi] X;Xiangtan Univ, Sch Math & Computat Sci, Xiangtan 411105, Peoples R China.
会议名称：
8th National Conference on Computational Mathematics
会议时间：
OCT 25-29, 2007
会议地点：
Sichuan Univ, Sichuan, PEOPLES R CHINA
会议主办单位：
[Zhong LiuQiang;Shu Shi] Xiangtan Univ, Sch Math & Computat Sci, Xiangtan 411105, Peoples R China.^[Zhong LiuQiang;Shu Shi] Hunan Key Lab Computat & Simulat Sci & Engn, Xiangtan 411105, Peoples R China.^[Sun Dudu] Chinese Acad Sci, Grad Univ, Acad Math & Syst Sci, Inst Computat Math & Sci Engn Comp, Beijing 100190, Peoples R China.^[Tan Lin] Nanhua Univ, Dept Math Phys, Hengyang 421001, Peoples R China.
关键词：
preconditioner;higher order edge finite element;stable decomposition
摘要：
In this paper, we are concerned with the fast solvers for higher order edge finite element discretizations of Maxwell’s equations. We present the preconditioners for the first family and second family of higher order Nédélec element equations, respectively. By combining the stable decompositions of two kinds of edge finite element spaces with the abstract theory of auxiliary space preconditioning, we prove that the corresponding condition numbers of our preconditioners are uniformly bounded on quasi-uniform grids. We also present some numerical experiments to demonstrate the theoretical results.
