Table of Content

05 April 2012, Volume 32 Issue 4

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Construction and identification of luciferase reporter gene vector

2012, 32(4):  338-341. 

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Objective To construct luciferase reporter gene vector containing human MLH1 promoter and to assay the transcriptional activity of hMLH1 promoter induced by E2. Methods hMLH1 promoter（-1953/+53）were amplified from the genomic DNA of human by PCR and cloned into luciferase reporter gene vector, pGL3-Basic. The recombined vector was transfected into HEK293 cells, and the activity of the luciferase was determined after the cells were simulated by E2 or not. Results The results of restriction enzyme digestion and sequencing indicated that the recombinant vector pGL3-Promoter1-luc was successfully constructed. After transcription of pGL3-Promoter1-luc, the activity fold of the luciferase was 7.45±0.81 induced by E2, which is significantly higher than 3.28±0.19 without E2(n=3,P<0.001). Conclusion The hMLH1 promoter contains the regulatory sequence associated with E2.

The role of mismatch repair gene hMLH1 in estrogen-induced colon cancer cell apoptosis

2012, 32(4):  342-345. 

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Abstract: Objective Exploring the role of mismatch repair gene hMLH1 played in the estrogen-induced colon cancer cell apoptosis. Methods: Transmit wild-type hMLH1-cDNA plasmid into hMLH1-deficient colon cancer cells (HCT116 cells) then treat cells with different concentrations of estrogen. Detect the rate of apoptosis and the activity of cells with flow cytometry and cell counting kit-8 respectively; Results:With the no-transfection group compared, after transfection , Estrogen can decreased the the activity and increase the apoptosis rate of HCT116 cells obviously .Conclusion: hMLH1 is involved in estrogen-induced apoptosis of colon cancer cell line HCT116.

Knocked down mismatch repair gene hMLH1 could influence microsatillite stability in human embryonic kidney cell line

2012, 32(4):  346-349. 

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Abstract: Objectinve To explored the ralations between expression of MLH1 gene and microsatillites stability in human embryonic kidney cell line 293t. Methods A plasmid vector encoding shRNA targeting hMLH1 (pGPU6/GFP/Neo-shMLH1) was constructed to knock down hMLH1 gene in 293t cell line，and evaluated the microsatallite stability before and after Knocked down. Results the expression of MLH1 in knocked down group was obviously knocked down in 293t cell, and the microsatallite states was changed from microsatallite stability into microsatallite instability conpared with control group. Conclusion The results showed that the expression of MLH1 gene was intimately associated with the microsatallite stability， knocked down hMLH1 protein could lead to microsatallite instability in cell line 293t.

Effects of ADMA on the expression of acyl-coenzyme A:Acylcholesterol transferase-1(ACAT-1) in cell differentiation from mononuclear/macrophage cells to foam cells.

2012, 32(4):  350-353. 

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[Abstract] Objective To investigate the effects of Asymmetric dimethylarginine(ADMA) on the expression of acyl-coenzyme A:acylcholesterol transferase-1(ACAT-1) in cell differentiation from mononuclear/macrophage cells to foam cells. Methods (1) Cultured THP-1 monocyte cell was induced into macrophages by 160nmol/L PMA for 48h and then incubated with 80mg/L ox-LDL for 24h macrophages were induced to foam cells. Transmission light microscope(using red oil O staining technique) was applied to appraise the morphology and change of foam cells．(2)After 20μmol/L ADMA was incubated with THP-1 monocyte cells，macrophage cells and foam cells for 24h, the cholesterolester content of foam cells was measured by enzyme assay. The expression of ACAT-1 in mRNA and protein were measured by means of RT-PCR and Western blot respectively. Results (1)ADMA could increase the cholesterolester content of foam cells.(2)Compared with the monocyte cells, expression of ACAT-1 in mRNA and protein in macrophage cells(p<0.05) and foam cells(p<0.01) obviously increased. Compared with the macrophage cells, expression of ACAT-1 in mRNA and protein in foam cells increased without significant difference.(3)Compared with the control group respectively treatment of monocyte cells, macrophage cells and foam cells with ADMA result in an increase in mRNA and protein levels for ACAT-1(p<0.01). Conclusion ADMA might increase the cholesterol content of foam cells via upregulating the expression of ACAT-1 in the mRNA and protein.

Effect of P53 shRNA on proliferation of hepatoma cell

2012, 32(4):  354-358. 

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Objective To observe the effect of P53 shRNA on the proliferation and expression of P21 protein in SMMC-7721 cell line. Methods Design short hairpin RNA(shRNA) sequences targeting human wild type P53 gene and construct recombinant plasmid pGPU6/GFP/Neo-P53 shRNA. SMMC-7721 cells were transfected with the recombinant plasmid and negative control vector respectively. Stably expressing clones were selected using G418. The proliferation was detected with clone form assay. The expression of P53 and P21 mRNA and protein were detected by RT-PCR and Western blot, respectively. SMMC-7721 cells were transplanted by subcutaneous injection to form transplantation tumor in nude mice. Then pGPU6/GFP/Neo-P53 shRNA or negative control shRNA were injected into implanted tumors directly, and tomor volume and weight were detected. Results P53 shRNAs, including P1, P2 and P3, can severely decrease P53 mRNA levels(P<0.05, P<0.05 or P<0.01). The clone form efficiency was increased significantly after interfering P53 function in SMMC-7721 cells(P<0.05), and the expression of P21 mRNA and protein were obviously decreased following the interference of P53 (P<0.05). After P53 was silenced, tomor volume and weight were increased significantly(P<0.05). Conclusion P53 shRNA silencing P53 to lower P21 protein expression may make SMMC-7721 hepatic carcinomas cells malignant proliferation.

Oxidative stress up-regulates the expression of β-Amyloid precursor protein cleavage enzyme 1 in SH-SY5Y human neuroblastoma cells

Liang LI

2012, 32(4):  359-362. 

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ABSTRACT : Objective To investigate the role of oxidative stress in the expression of β-Amyloid precursor protein cleavage enzyme 1(BACE1) and the changes of DNA methylation and histone acetylation.Methods Cultured SH-SY5Y cells treated with H2O2 were used to test the expressions of BACE1, DNA methyltransferases 1, 3A (DNMT1,DNMT3A) and histone deacetyltranferase (HDAC) by Western blot. The level of mRNA of BACE1 was assessed by RT-PCR. Acetylation level of histone H3 and H4 were examined by optical density assay. Results Both BACE1 mRNA and protein levels were up-regulated significantly after H2O2 treatment for 1 and 72h; DNMT1 and DNMT3A expressions were decreased to 75% and 65% of control respectively after H2O2 treatment for 72h; HDAC3 level was increased as 1.6 folds as control; While the level of histone H3 acetylation was decreased and there was no change with histone H4 acetylation. Conclusion Oxidative stress may regulate BACE1 expression in SH-SY5Y through alteration of DNA methylation and histone acetylation which play a role in Alzheimer's disease(AD) pathogenesis.

Islet-1 specifically assisted the process of C3H10T1/2 cells differentiating into cardiomyocyte-like cells in the histone acetylation regulatory network

2012, 32(4):  363-368. 

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Objective To find out which proteins of histone acetylase (HATs) and histone deacetylase (HDACs) interact with Islet-1 during the differentiation of C3H10T1/2 cells transfected with Islet-1 lentiviral vector into cardiomyocyte-like cells, and to confirm the pivotal role of Islet-1 in the network of histone acetylation. Methods Culture and observe C3H10T1/2 cells transfected with Islet-1 lentiviral vector. The position of Islet-1 was detected by Immunofluorescence cytochemistry. The protein extraction time was determined by Western-blot according to expression levels of Islet-1-immunoprecipitation. The Islet-1-binding protein was precipitated by Co-immunoprecipitation-polyacrylamde (Co-IP). The proteins of HATs and HDACs interacting with Islet-1 were verified by Western-blot. Results Cells in induction group showed the appearance of cardiomyocyte-like cells. The location of Islet-1 was in cytoplasm. The protein extraction time in induction group was significant in the third week (0.782±0.015) compared with the first 2 weeks. The expression of Islet-1 in induction group was significantly higher than that in blank control group and C3H10 group (0.819±0.026，0.127±0.006 and 0.126±0.001 respectively, P<0.05）.The proteins interacting with Islet-1 were GCN5、P300/CBP and HDAC4. Conclusions The synergism of Islet-1 and its interacting proteins such as GCN5、P300/CBP and HDAC4 played a specific assisting role in the differentiation of C3H10T1/2 cells into cardiomyocyte-like cells.

EKLF activates the expression of miR-96 during erythroid differentiation

2012, 32(4):  369-374. 

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Abstract：Objective To study the regulation of Erythroid Kruppel-like factor (ELKF) on the expression of miR-96 in Erythropoiesis. Method K562 cells were induced to erythroid differentiation by Hemin. The expression of miR-96 during erythroid differentiation was detected by real-time PCR. Bioinformatic analysis was used to search for binding sites for EKLF within 2kb upstream sequence of transcriptional start site (TSS) of miR-96. Biology function of these sites were detected by ChIP-PCR combined with Dual-Luciferase Reporter Assay. Result miR-96 expression was increased during erythroid differentiation of k562 cells induced by Hemin and peaked at 48h (3.94156±0.63995, p<0.05). Several binding sites within 2kb upstream sequence of TSS of miR-96, occupied with EKLF can recruit RNA polymerase II (Pol II) and promote the expression of downstream genes. Conclusion EKLF activates the expression of miR-96 in Erythropoiesis directly.

The analysis of the factors induced rat mesenchymal stem cells tumorigenesis in vitro simulated tumor microenvironment

2012, 32(4):  375-380. 

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Objective To investigate the relation between marrow mesenchymal stem cells tumorigenesis and tyrosine kinase signaling molecules such as HGF、IL-6，BFGF in vitro .Methods The tumor microenvironment was simulated by co-culture MSCs with C6 and the normal microenvironment was simulated by co-culture MSCs with astrocytes; MSCs were divided into three groups:Experimental group(co-cultured with C6), Control group (co-cultured with astrocytes) Blank control group ( MSCs alone) ；P53 and MDM2 of MSCs in each group were measured by PCR, Western blotting ；HGF，IL-6 and BFGF expression in each group were detected by ELISA ; the STAT3 protein expression of MSCs treated with corresponding ELISA amount tyrosine kinase signaling molecule were detected by immunofluorescence. Results Experimental group cells showed tumor cell-like morphology. MDM2 mRNA in experimental group was the control group 1.56±0.21 fold(P<0.05);MDM2 protein in experimental group increased 90±7% as compared to control group (P<0.01)；P53 mRNA decreased to 0.55±0.10 and the level of mutant P53 protein increased to 87±5% in experimental group as compared to control group (P<0.01); HGF and IL-6 significantly increased in Experimental group as compared to Control group (P<0.05). P-STAT3 expression increased in IL-6 overdose group as compared to IL-6 normaldose group. (P<0.01). Conclusion IL-6 can induce mesenchymal stem cells tumorigenesis in vitro simulated tumor microenvironment.

Establishment of 293-siDrosha stable cell line and detection of its potential use in the study of microRNA functions

2012, 32(4):  381-385. 

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Abstract：Objective To construct Drosha-1 deficient 293 stable cells (293-siDrosha) and to study microRNA processing by using the established 293 stable cells. Methods The pSicoR-human Drosha1 plasmid DNAs were transfected into 293 cells and selected for neomycin resistant clones with 1200g/ml G418 for 2-3 weeks. The mRNA and protein expressions of Drosha were detected by RT-PCR，real-time PCR and Western blotting. The expressions of hsa-miR-491-5p in 293 cells, uncloned 293-siDrosha cells (293-siDrosha mixed) and the cloned 293-siDrosha cells (293-siDrosha #3 cells) were detected with poly(A) real-time RT-PCR. Results Compared with the control cells, the mRNA and protein expressions of human Drosha1 in cloned 293-siDrosha cells were dramatically decreased. The expression levels of hsa-miR-491-5p in the cloned 293-siDrosha cells have about 120 fold reduction as compared with that of the control cells. Conclusion 293-siDrosha stable cells were successfully constructed. The cloned 293-siDrosha cells may be useful as a model system for the study of microRNA functions.

A study of the acute pulmonary injury effects of metal oxide materials in mice

2012, 32(4):  386-389. 

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Abstract: Objective To compare and evaluate the pulmonary toxic potential of metal oxide nanoparticles (NPs), including copper oxide, ferric oxide, titanium oxide and silica in C57/BL6 mice. Methods C57/BL6 mice were exposed to metal oxide NPs via intra-tracheal instillation. Mice survival rate, lung wet-dry ratio and the expression level of cytokines in mice BAL fluid were evaluated. Results All mice died within 24 h after administration of high dose copper oxide NPs, while no mice was found dead when the same dose of the other metal oxide NPs were administered. Mice exposed to copper oxide also had significantly higher lung wet-dry ratio and higher interleukin-6 expression level in BAL fluid compared to control group. The administration of the other metal oxides did not result in significant increase of lung wet-dry ratio or elevation of IL-6 in BAL fluid compared to control group. Conclusion Copper oxide NPs demonstrated high lethality in C57/BL6, and can cause pulmonary edema, resulting in acute lung injury. In comparison, the other metal oxide NPs have much lower toxic potential and have little pulmonary injury effect in mice at the doses we used. High expression of IL-6 may play an important role in copper oxide NP-induced acute lung injury.

Effect of bone marrow mesenchymal stem cells transplantation on angiogenesis and proliferation-apoptosis in ischemic myocardium

2012, 32(4):  390-395. 

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Objective To investigate the effects of bone marrow mesenchymal stem cells (BMSC) transplantation on angiogenesis and proliferation-apoptosis in ischemic myocardium. Methods BMSC isolated from male mice were transfused into female mice with isoproterenol-induced myocardial ischaemia via tail vein. This study included three groups: BMSC, untreated, and control groups. Five weeks after treatment, expression levels of sex-determining region of Y-chromosome (SRY) and vascular endothelial growth factor (VEGF) in myocardium were detected by fluorescent qRT-PCR. Collagen distribution was observed using sirius red staining. The protein expression of VEGF, proliferating cell nuclear antigen(PCNA) and caspase-3 was detected by immunohistochemistry. Results BMSC group had significantly higher expression of SRY （11.22±0.90 vs 1.05±0.47, P<0.05）. Compared with the untreated group, BMSC group had decreased levels of collagen content(3.44±0.84 vs 8.44±1.09, P<0.05) and caspase-3（0.46±0.11 vs 3.12±0.28, P<0.05）, and increased level of VEGF(14.19±0.37 vs 11.88±0.28, P<0.05) and PCNA(4.08±0.18 vs 0.64±0.05, P<0.05). Conclusion BMSC can home to ischemic myocardium. BMSC transplantation improve microvascular angiogenesis and regulate the proliferation and apoptosis in ischemic myocardium.

Gene profiling of skin fibroblasts with silenced PTGS2 reveals a tendency toward keloid development

2012, 32(4):  396-401. 

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Objective Keloids are benign fibroproliferative dermal tumors developing as a result of pathological wound healing responses. The key alterations responsible for the pathogenesis of keloids are still poorly understood and there is no satisfactory treatment for this disorder. This study sought to elucidate the pathogenesis of keloid from the aspect of PTGS2 alteration and to find out potential targets for therapy. Methods Skin fibroblasts, the major inductive cell for keloid formation, were transfected with a recombinant PTGS2 siRNA expression vector. Real-time RT-PCR was used to confirm the knock down efficacy of PTGS2 siRNA. We performed gene expression analysis of the fibroblasts transfected with PTGS2 siRNA expression vector in comparison with the fibroblasts transfected with control vector using cDNA microarray chip which comprised of 21,552 clones. Different expression genes were annotated with literature mining method. Results The results of real-time RT-PCR indicated that recombinant PTGS2 siRNA expression vector could significantly knock down the expression of PTGS2 gene. We observed differential regulation of approximately 189 genes of the 10,682 efficient genes data in cDNA microarray，according to the data-filter-standard of 1.5 fold, of which 115 genes were up-regulated and 74 genes were down-regulated when compared with control. 14 genes were differently expressed between transfected fibroblast and control according to the standard of 2 fold, of which 9 genes were up-regulated and 5 genes were down-regulated. Conclusions The results imply that PTGS2 is one of the key alterations responsible for keloid formation and that PTGS2 provide a potential target for therapy of keloid.

Research on the Helicobacter pylori-induced autophagy in human gastric epithelium (GES-1)

2012, 32(4):  402-406. 

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Abstract:Objective Make an observation of the autophagy induced by H. pylori infection in human gastric epithelium（GES-1）Methods Optimal multiplicity of infection (m.o.i) of H .pylori was determined by neutral red uptake method (NRU). GES-1 was infected by H. pylori with different time. Autophagy induced by H. pylori was interfered with 3MA, E64d and pepstatin A. Western blot was utilized for detecting the level of LC3 conversion and p62, which indicated the autophagy induction. The formations of autophagosomes were observed via immunofluorescence Results The optimum m.o.i was 400 for H. pylori (22695) infecting GES-1. At 2h p.i, autophagy was detected. It reached a peak level at 8h p.i, while it returned to the basic level at 24h p.i. 3MA was able to inhibit autophagy with obviously decrease of autophagosome formation. And E64d and pepstatin A could block autophagy downstream to some extent Conclusion H. pylori is capable of inducing autophagy in human gastric epithelium (GES-1), which can be regulated by autophagic inhibitors.

The effect of tetramethylpyrazine on the expression of NF-kB and I-kBα after acute spinal cord injury in the rat model

2012, 32(4):  407-412. 

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Abstract: Objective To study the effect of Teramethylpyrazine (TMP) on expression of NF-kB and I-kBα in acute spinal cord injury(ASCI) in rats. Methods Allen’S weight drop method was used to establish acute spinal cord injury(SCI) rat model at T10 section and was conducted in 110 adult Sprague Dawley rats that were subsequently divided into Sham operation group (group S， n=10)；Control group (group C，n=50)；Tramethylpyrazine group (group T，n=50). The function of spinal cord was evaluated with animal behavioral scores by measuring modified Rivilin loxotic plate test and counting BBB and CBS score at 1、3、5、7、14and 21d postoperatively．The injured spinal cord tissue samples were harvested at 1h、3h、6h、12h、1d、3d、5d、7d、14d and 21d postoperatively(n=5 for each time point) for the preparation of continuous histological sections that were analyzed the expression of NF-kB and I-kBα by immunohistochemistry method．Results T group had significantly higher degrees than C group at 7、14 and 21 days in modified Rivlin loxotic plate test after SCI (p＜0.05)；T group had significantly higher scores in BBB score than C group at 5、7、14 and 21 days after SCI respectively(p＜0.05).C group had significantly higher scores in CBS score than T group at 5、7、14 and 21 days after SCI respectively(p＜0.05). The number of NF-kB positive cells were significantly lower in T group than C group at 1、3、5 and 7 days after SCI(p＜0.05); The number of I-kBα positive cells were significantly lower in C group than T group at 1、3、5 and 7 days after SCI(p＜0.05). Conclusion The TMP can promote the repair of injured spinal cord tissue through increasing the I-kBα expression and decreasing the NF-kB expressions in cells after ASCI.

Rhein lysinate induces apoptosis in human cervical cancer CaSki cells by inhibiting EGFR signal pathway

2012, 32(4):  413-416. 

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Comparative analysis of plasma proteome of early and advanced stage of cervical carcinoma of Uighur women by two-dimensional liquid phase chromatography

2012, 32(4):  417-422. 

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Objective To analyze the proteomic profile of low abundant plasma proteins in cervical squamous cell carcinoma（CSSC）of Uighur women by using two dimensional liquid phase chromatography, to identify differences of plasma proteome between early and advanced stages of the cancer. Methods Forty-six cases of plasma samples from Uighur women with CSSC were collected，including 26 cases of early stage cancer atⅠ-Ⅱa and 20 cases of advanced stage cancer at Ⅱb-Ⅳ; After preparation of the proteome of low abundant plasma proteins by depletion of high abundant proteins, the proteomic fingerprint features of patients with early stage and advanced stage of cancer were studied by two-dimensional liquid phase chromatography (ProteomeLabTM PF- 2 D) , to establish a distinguishing model of plasma proteome for patients withdifferent stages of cancer. Results A plasma proteome fingerprint model specific to patients with early stage and advanced stage of cancer was established. By setting up the protein content difference of more than two times as a standard for quantitative differences, 5 peaks with ascending and 10 with descending protein content in patients with advanced stage of cancer compared to early stages were found. Conclusion The remarkable difference in low abundant plasma proteomes between early and advanced stages of CSCC in Uighur women may provide an important evidence for the identification of plasma protein markers specific to the cancer progression in the future.

JAK/STAT pathway mediates IL-4-induced collagen type I expression in human hepatic stellate cells

2012, 32(4):  423-427. 

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Aim To investigate the effects of IL-4 on collagen type I mRNA expression and protein production, and the roles of Janus kinase/signal transducers and activators transcription(JAK/STAT) signaling transduction pathway in increased collagen type I mRNA expression stimulated by IL-4 in activated hepatic stellate cells(HSCs). Methods First, collagen type I mRNA expression and protein production induced by IL-4 at different doses in a human HSC cell line, LX-2 was determined by RT-PCR and ELISA. Second, the effects of JAK inhibitor AG490 on JAK1 phosphorylation and collagen type I mRNA expression stimulated by IL-4 were detected by Western blot and RT-PCR. Third, the roles of transfection with STAT6 antisense oligonucleotide (STAT6-ASON) in STAT6 phosphorylation after IL-4 were detected by Western blot. Finally, the effect of transfection with STAT6-ASON on collagen type I mRNA expression after IL-4 was measured by RT-PCR. Results IL-4 increased collagen type I mRNA expression and protein production in a dose-dependent manner in LX-2, reaching a maximal level at 50 ng/ml IL-4. In addition, JAK inhibitor AG490 completely blocked JAK1 and STAT6 phosphorylation and increase in collagen type I gene expression after IL-4 in LX-2. Transfection with STAT6-ASON blocked STAT6 phosphorylation and increased collagen type I mRNA by IL-4 in LX-2. Conclusion JAK/STAT signaling pathway had mediated IL-4-induced collagen type I mRNA expression and protein production in activated HSC.

Effect of different stress on the expression of BDNF and BDNF mRNA in the hippocampus of rats

2012, 32(4):  428-432. 

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ABSTRACT : Objective To study change of BDNF expression in hippocampus and prefrontal lobe of rats by acute and chronic forced-swimming stress , and study the effect of different intensity stress on the behaviors of rats. Method After different intensity stress by forced swimming in the water, the change of BDNF mRNA expression in hippocampus was observed by RT-PCR, and Western blotting was used to explore the expression of BDNF protein in rat hippocampus. Result Acute stress resulted in elevated expression of BNDF mRNA and protein, and the expression of BDNF became lower and lower after 3 hours . Meanwhile the chronic stress led to the lower level expression of the BDNF compared with acute group in many time points (p<0.05).Conclusion Acute stress resulted in the high level expression of BDNF in hippocampus. Chronic repeated stress led to the habituation expression of BNDF, which was lower than that of acute stress group.

Research of Serum Proteome Profiling of Pancreatic Adenocarcinoma by ProteoMiner Beads Enrichment of Low Abundance Protein

2012, 32(4):  433-436. 

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[Abstract] Objective: To investigate the expression and clinical significance of eight proteins in pancreatic adenocarcinoma. Methods: The present study used ProteoMiner beads to treat neat serum sample of pancreatic cancer and control followed by two-dimension gel and ESI-MS/MS to identify the signature proteins involved in pancreatic carcinogenesis. ELISA was used to determine serum level of clusterin. Results: We found that seven proteins, which includes clusterin, vitronectin, complement C4-A, vitamin D-binding protein, anitthrombin-III, complement component C and prothrombin, is up-regulated and complement component C7 is down-regulaed in serum of pancreatic cancer. ELISA results showed that serum level of clusterin enhanced in pancreatic adenocarcinoma significantly. Conclusion: Clusterin may correlate closely with development and evolution of pancreatic adenocarcinoma and serum level of clusterin could be a key biomarker for diagnosis of pancreatic adenocarcinoma.

Expression of FGF10 and FGFR2Ⅲb in development of mouse kidney

2012, 32(4):  437-441. 

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Abstract：Objective To observe the expression and sites of FGF10 and FGFR2 Ⅲb during kidney development of mouse, in order to investigate their roles in kidney development. Methods Immunohistochemistry technique and Western blotting method were used to observe the expression of FGF10 and FGFR2 Ⅲb at embryonic day 12、14、16、18 and neonatal day 1、7、14、21、42 in the developing mouse kidney. Results FGF10 and FGFR2 IIIb were weakly expressed in the ureteric buds at E12d and then with the renal development, FGF10 and FGFR2 IIIb were expressed mainly in distal tubules and collecting ducts. FGF10 was expressed also in the proximal convoluted tubule. FGFR2 IIIb was not expressed in the proximal tubule. The renal corpuscles in each development stage were not found the expression of FGF10 and FGFR2 IIIb. Western blot showed that during kidney development, the expressions of FGF10 and FGFR2 IIIb were increased firstly and then decreased. Conclusions FGF10 and FGFR2 IIIb probably play an important role in the renal development.

The Clinical Findings and Imaging Features of Retroperitoneal Fibrosis Secondary to Malignant Neoplasmas

2012, 32(4):  442-446. 

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Abstract: Objective To analyze the clinical and imaging features of retroperitoneal fibrosis (RPF) secondary to malignant tumors. Methods We retrospectively analyzed 106 patients with retroperitoneal fibrosis from July 1992 to January 2010 in our hospital. Among them 8 cases with malignant tumors were consecutively enrolled in the study. The demographic and clinical data of the 8 patients were collected, and the follow-up was fulfilled regularly. Results We found that there were 5 male and 3 female among the patients, and the mean age was 59.6 years old. The primary neoplasms were from genital system (4 cases), digestive system (2 cases), hematological system (1 case) and malignant neurilemmoma (1 case). One case underwent both the stomach carcinoma and bladder cancer. The clinical symptoms of malignant RPF had no typical features compared to those of the benign RPF. However, the abdominal X-ray computed tomography (CT) exposed some important features which were special to the malignant RPF. If the RPF masses are very extensive, elevate aorta and ureter from spine, or have a lobulated anterior margin, which clue to the malignant diagnosis. In the meanwhile , the abdominal CT can evaluate the management effectiveness and prognosis. Definite diagnosis of the RPF mass depends on the pathology findings. Conclusion Familiarity with the imaging manifestations of retroperitoneal fibrosis is vital to differential diagnosis.

Gene Mutation Analysis Of The Rh WeakD And DEL Phenotype

2012, 32(4):  447-450. 

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Abstract Objectives To investigate the molecular basis of the Rh weak D and DEL phenotype Methods Weak D and DEL phenotype expression were screened out with an indirect anti-human globulin test(IAT) and absorption elution test.Then the nucleotide sequences of ten exons of weak D and DEL phenotype were evaluated by a RHD gene-specific PCR-SSP and sequencing. Results Indicated that weak D phenotype harbored a RHD 845G >A mutation in exon 6 and harbored a 282Gly>Asp amino acid mutation in the ninth transmembrane and cytoplasmic regions of RhD prtione ,but DEL phenotype harbored a RHD 1227G >A mutation in exon 9 and this mutation is silence. Conclusion The RHD gene sequencing method is established , the molecular basis of weak D and DEL phenotype is characterized ,and this study is the basis for discovering the new D variation phenotypes and new RHD alleles．

A case report of mixed epithelial and stromal tumor of the kidney

2012, 32(4):  451-452. 

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The IL23/IL17 axis in the immunopathogenesis of psoriasis

2012, 32(4):  453-456. 

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Abstract：Abnormal activated T cells infiltration and cytokine production are predominant mediators of skin pathology in psoriasis, a chronic inflammatory skin disease. Psoriasis has been definited as a T helper (Th) 1-type disease mediated by IL-12 、IFN-γ、TNF-α. Recently, Accumulating evidence suggests that IL-23 and the subsequent Th17 cell response it promotes are central factors in the pathogenesis of this disease.IL-23 is a central growth factor for Th17 cells as it influences both their differentiation and expansion.Th17-related cytokines including IL-17、 IL-21、IL-22 play a functional role in psoriasis and other Autoimmune diseases.

The effect and related mechanism of cancer stem cell in tumor metastasis: new perspective and progress

2012, 32(4):  457-460. 

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Metastasis is the major cause of death for cancer patients. Further insights have been put into the biology of metastasis. Recently, with the growing support for the cancer stem cell (CSCs) hypothesis and probing into the properties of CSC and related field, more and more evidences suggest CSCs as candidates for mediating metastatic progression. The importance of CSCs in tumor-initiation has been firmly established in leukemia and other solid tomors. However, the role of CSCs in multistage cancer progression, particularly with respect to metastasis, has not been well-defined. Studies have suggested the epithelial-mesenchymal transition (EMT), tumor microenvironment and angiogenesis in regulating cancer metastasis. Current research has also highlighted the above related mechanism in mediating CSC metastasis. The purpose of this review is to discuss recent advances in the field of CSC metastasis and related mechanism.