Biomedical subjects

Yi Zhu

Publications and source records attributed to Yi Zhu.

63 records · Page 4Linked to original sources

PubMed2003

Type two hyper-IgM syndrome caused by mutation in activation-induced cytidine deaminase.

Thirteen Japanese patients with hyper-IgM syndrome but normal CD40 ligand were characterized. All patients had mutations in AID (activation-induced cytidine deaminase) gene. Five of them had a missense mutation of Arg112His. In all patients, serum IgG, IgA and IgE levels were undetectable, B cells failed to produce detectable amounts of IgE even if cultured them with anti-CD40 and IL-4. Somatic hypermutation (SHM) was also impaired in their peripheral blood B cells. These results suggest that Arg112 is the hot spot of AID mutation and demonstrate that AID plays indispensable roles in class switch recombination (CSR) and somatic hypermutation (SHM) in human B cells. In addition, serum IgM levels in the patients have been continuously high even after proper intravenous immunogloburin infusion (IVIG) and without infection, indicate that AID has the function to induce spontaneous IgM production in B cells.

Adult↗

PubMed2003

[Significances of plasma levels of neuropeptide Y pre- and post-treatment in patients with decompensated cirrhosis and ascites].

OBJECTIVE: To observe changes of plasma neuropeptide Y(NPY) level in ascitic patients with decompensated cirrhosis pre- and post-treatment, there fore to understand the correlation of NPY with liver function and ascitic formation. METHODS: NPY plasma levels in 20 patients with decompensated cirrhosis and ascites were detected by radioimmunological assay. RESULTS: Plasma NPY levels in patients with cirrhotic ascites were significantly lower than those in normal subjects(P < 0.01) in spite of the increases of NPY after ascites decreased (P < 0.01), which were still lower than those in normal subjects(P < 0.01). CONCLUSION: Decreased plasma NPY levels are correlated with the severity of liver damage and may be responsible for the changes of hemodynamics and ascitic formation in patients with liver cirrhosis.

Adult↗

PubMed2003

[Effects of quercetin on platelet-endothelial cell adhesion and their expression of adhesion molecules].

AIM: To observe the effect of quercetin (Que) on the adhesion of platelets to cultured endothelial cells and adhesion molecule expression by human umbilical vein endothelial cells (HUVEC) and platelets. METHODS: [3H]-Adenine labeled platelets were incubated with HUVEC to investigate the effect of Que on adhesion of platelets to HUVEC. The number of platelets adhering to the HUVEC monolayer was determined by liquid scintillation spectroscopy. TNF-alpha induced HUVEC expression ICAM-1 and thrombin induced platelets expression of P-selectin were measured by flow cytometry. RESULTS: Que (0.3-2.4 mumol.L-1) was shown to inhibit the increase of P-selectin expression of thrombin activated platelets. Pretreatment of HUVEC with tumor necrosis factor (TNF-alpha) significantly increased platelets adhesion to HUVEC and the expression ICAM-1. Que (0.6-2.4 mumol.L-1) inhibited this effect of TNF-alpha in a concentration-dependent manner. CONCLUSION: Que can inhibit the adhesion of platelets to HUVEC and the expression of adhesion molecules (P-selectin and ICAM-1).

Blood Platelets↗

PubMed2003

Inhibitory effect of quercetin on proliferation of human microvascular endothelial cells in vitro.

AIM: To investigate the role of quercetin (Que) in the proliferation of cultured human skin microvascular endothelial cells (MVEC). METHODS: Cell count and [methyl-3H]thymidine ([3H]TdR) uptake assay were used to measure the effect of Que in the proliferation of cultured MVEC. Cytotoxicity of Que on MVEC was also evaluated by 51Cr release assay. RESULTS: When MVEC were treated with Que, the proliferation was significantly inhibited in a time-course and dose-dependent manner. Que 5 micromol/L did not inhibit the proliferation of MVEC. When the concentration of Que increased to 20, 40, 80, and 160 micromol/L, the cell numbers per well were decreased and the inhibition rate was 12.2 %, 23.5 %, 35.3 %, and 54.1 % respectively with IC50 of 138 micromol/L. The inhibitory rate of [3H]-TdR uptake was 18.7 %, 34.4 %, 48.9 %, and 62.5 % respectively (IC(50)=87.5 micromol/L). (51)Cr release assay showed that Que 160 micromol/L incubated with MVEC from 1 to 16 h had no clear cytotoxicity compared with control group. CONCLUSION: Que greatly inhibited the proliferation of cultured human MVEC in vitro. This effect may not be related to the cytotoxicity of Que on MVEC.

Cell Division↗

PubMed2002

Analysis of altered genomic expression profiles in the senescent and diseased myocardium using cDNA microarrays.

Cardiac function deteriorates with aging or disease. Short term, any changes in heart function may be beneficial, but long term the alterations are often detrimental. At a molecular level, functional adaptations involve quantitative and qualitative changes in gene expression. Analysis of all the RNA transcripts present in a cell's population (transcriptome) offers unprecedented opportunities to map these transitions. Microarrays (chips), capable of evaluating thousands of transcripts in one assay, are ideal for transcriptome analyses. Gene expression profiling provides information about the dynamics of total genome expression in response to environmental changes and may point to candidate genes responsible for the cascade of events that result in disease or are a consequence of aging. The aim of this review is to describe how comparisons of cellular transcriptomes by cDNA array based techniques provide information about the dynamics of total gene expression, and how the results can be applied to the study of cardiovascular disease and aging.

Cardiovascular Diseases↗

PubMed2002

Shear stress activation of SREBP1 in endothelial cells is mediated by integrins.

We investigated the effect of shear stress on the sterol regulatory element-binding protein 1 (SREBP1) in vascular endothelial cells (ECs) and the mechanotransduction mechanism involved. Application of a shear stress (12 dyn/cm(2)) caused the proteolytic cleavage of SREBP1 and the ensuing translocation of its transcription factor domain into the nucleus. As a result, shear stress increased the mRNAs encoding the low density lipoprotein receptor (LDLR), as well as the binding of (125)I-LDL. Using a step flow channel, we showed that SREBP1 activation in ECs under laminar flow is transient, but disturbed flow causes sustained activation. In studying the shear stress-elicited molecular signaling that activates SREBP1, we found that blocking the beta(1)-integrin with the AIIB2 blocking-type monoclonal antibody inhibited SREBP1 activation induced by shear stress. EC attachment to fibronectin or the activation of beta(1)-integrin in the suspended ECs by the TS2/16 monoclonal antibody was sufficient for SREBP1 activation. Furthermore, transient transfection assays showed that dominant-negative mutants of focal adhesion kinase and c-Src attenuated the shear stress-increased LDLR promoter activity. These results demonstrate that integrin signaling plays a critical role in the modulation of SREBP in ECs in response to shear stress.

Animals↗

PubMed2002

Native LDL upregulation of ATP-binding cassette transporter-1 in human vascular endothelial cells.

ATP-binding cassette transporter-1 (ABCA1) mediates the lipid efflux from cells to apolipoproteins. In studying the gene expression and regulation of ABCA1 in human vascular endothelial cells (ECs), we found that native low density lipoprotein (LDL) elevates ABCA1 in both protein and mRNA levels in a time- and dose-dependent fashion. Transfection of full-length human ABCA1 in ECs lowers cellular cholesterol content and increases apolipoprotein (apo) A-I-mediated cholesterol efflux. Transfection of the ABCA1 promoter-luciferase reporter results in a 2-fold induction after LDL exposure. The responsive element was mapped within -116 to -54 of the promoter region with use of promoter deletion constructs, as reported in other cells. A mutation of the DR4 site greatly diminished the LDL effect. Results showing that LDL increases the liver X receptor responsive element (LXRE)-driven luciferase activity demonstrate the effect of LDL on LXR activation. Furthermore, ligands of the retinoid X receptor and LXR activate ABCA1 in ECs at levels of both promoter activation and mRNA induction. Therefore, ABCA1 is expressed in vascular ECs and is transcriptionally upregulated by LDL. Overexpression of ABCA1 in these cells prevents overloading of cholesterol by increasing the efflux of cholesterol. Thus, ABCA1 plays an important role in the homeostasis of cholesterol in the vascular endothelium.

ATP Binding Cassette Transporter 1↗

PubMedDate not supplied

Quantitative analysis of EcoR1 methylase-DNA complex by atomic force microscopy.

The EcoR1 methylase specifically recognize 5'-GA* ATTC-3' in DNA duplex. We directly applied atomic force microscopy (AFM) to investigate linear pBR322-EcoR1 methylase complexes and quantitatively analyzed the bend angles of linear pBR322-EcoR1 methylase complexes and the bound protein widths. In this study, we made a novel observation that DNA-EcoR1 methylase complexes exhibited two populations of conformation at recognition site: DNA bent an acute angle at the recognition site in the presence of one EcoR1 methylase monomeric molecule, while DNA bent an unacute angle at the recognition site and the complementary site on duplex DNAs in the presence of EcoR1 methylase dimer. The data indicated that the unacute angle state was the result of unique interactions between EcoR1 methylase and the recognition site and the complementary site on duplex DNAs, and suggested that the acute angle conformation could be an intermediate in the formation of the unacute angle state. Our works provide a detail insight into the DNA structural variations involved in EcoR1 methylase-binding processes and demonstrate further the versatility of AFM as an imaging technique for studying the interaction between large DNA fragment and protein.

Binding Sites↗

PubMedDate not supplied

HeLa cell adhesion on various collagen-grafted surfaces.

Cell adhesion is important to develop cell microarrays and biocompatible materials. Collagen has been reported to be able to improve cell adhesion. In this paper, two collagen coating methods (collagen grafted directly on the substrate and chitosan-modified substrate) were carried out, on which the adhesive behaviors of HeLa cells were studied. An atomic force microscope and a surface potential meter were used to characterize morphologies and electric polarization of these surfaces. It was found that surface electric polarization and the its durability and surface topography were key factors to cell adhesion. Collagen (1 mg/mL) grafted on 1% chitosan-modified surface showed the best adhesion of HeLa cell. This work might be helpful to the practical application of cell microarray chips.

Cell Adhesion↗