Biomedical subjects

Guo Wei

Publications and source records attributed to Guo Wei.

22 records · Page 2Linked to original sources

PubMed2004

[Study of biosensor technology on the detection of endotoxin-neutralizing materials].

OBJECTIVE: To explore the application of biosensor technology in the determination of endotoxin-neutralizing materials. METHODS: After mixing polymyxin B (PMB) with endotoxin in certain concentration, the neutralizing ratio of PMB to endotoxin was assessed by biosensor technique and limulus amebocyte lysate test respectively. The results from the two methods were compared. RESULTS: The neutralizing ratio of PMB to endotoxin as assessed by biosensor technology was 0.35 microg to 1 ng, while that by dynamic turbidimetric and chromogenic limulus amebocyte lysate (LAL) technique was 0.5 mg to 1 ng and 1 mg to 1 ng, respectively. The results obtained by biotechnology were similar to that by biosensor technique. CONCLUSION: Biosensor technology was an accurate, convenient and rapid method for the determination of potency of endotoxin-neutralizing materials.

Bacterial Proteins↗

PubMed2003

Hearts from rodents exposed to intermittent hypoxia or erythropoietin are protected against ischemia-reperfusion injury.

BACKGROUND: Preconditioning phenomena provide evidence for adaptive responses to ischemia that have important implications for treatment/prevention of myocardial infarction. Hypoxia-inducible factor 1 (HIF-1) mediates adaptive transcriptional responses to hypoxia/ischemia. METHODS AND RESULTS: Exposure of wild-type mice to intermittent hypoxia resulted in protection of isolated hearts against ischemia-reperfusion injury 24 hours later. Cardiac protection induced by intermittent hypoxia was lost in Hif1a+/- mice heterozygous for a knockout allele at the locus encoding HIF-1alpha. Erythropoietin (EPO) mRNA expression was induced in kidneys of wild-type mice subjected to intermittent hypoxia, resulting in increased plasma EPO levels. EPO mRNA expression was not induced in Hif1a+/- mice. EPO administration to rats increased functional recovery and decreased apoptosis in isolated hearts subjected to ischemia-reperfusion 24 hours later. CONCLUSIONS: Hearts isolated from rodents subjected to intermittent hypoxia or EPO administration are protected against postischemic injury. Cardiac protection induced by intermittent hypoxia is critically dependent on Hif1a gene dosage. Our data suggest that additional studies to evaluate therapeutic applications of EPO administration are warranted.

Animals↗

PubMed2003

Ets-2 and components of mammalian SWI/SNF form a repressor complex that negatively regulates the BRCA1 promoter.

Ets-2 is a transcriptional activator that can be modulated by ras-dependent phosphorylation. Evidence is presented indicating that ets-2 can also act as a transcriptional repressor. In the breast cancer cell line MCF-7, exogenous ets-2 repressed the activity of a BRCA1 promoter-luciferase reporter dependent on a conserved ets-2-binding site in this promoter. Conditional overproduction of ets-2 in MCF-7 cells resulted in repression of endogenous BRCA1 mRNA expression. To address the mechanism by which ets-2 could act as a repressor, a biochemical approach was used to identify proteins that interacted with the ets-2 pointed domain. From this analysis, components of the mammalian SWI/SNF chromatin remodeling complex were found to interact with ets-2. Brg-1, the ATP-hydrolyzing component of the SWI/SNF complex, along with the BAF57/p50 and Ini1 subunits could be co-immunoprecipitated from cells with ets-2. The pointed domain of ets-2 directly interacted in vitro with the C-terminal region of Brg-1 in a phosphorylation-dependent manner. The combination of Brg-1 and ets-2 could repress the BRCA1 promoter reporter in transfection assays. These results support a role for ets-2 as a repressor and indicate that components of the mammalian SNF/SWI complex are required as co-repressors.

3T3 Cells↗

PubMedDate not supplied

Ets-2 interacts with co-repressor BS69 to repress target gene expression.

BACKGROUND: The ETS-family of proteins consists of over 30 members that regulate the growth, differentiation and survival of both normal and tumor cells. How specificity is achieved within this family remains largely unresolved. One mechanism for attaining specificity is through the action of signaling pathways on specific family members. For example, Ets-2 is an activator modulated by ras-dependent phosphorylation of a single residue in the conserved pointed domain of this factor. We hypothesized that phosphorylation of the pointed domain regulates the proteins that can interact with ets-2 in the cell nucleus, resulting in regulation of target genes. MATERIALS AND METHODS: We used a combination of biochemical assays, yeast two-hybrid screens and transfection assays to identify and characterize proteins interacting with the pointed domain. RESULTS: BS69, a known co-repressor, was identified in a yeast two hybrid screen as an ets-2 interacting partner. BS69 can interact with ets-2 in vivo and phosphorylation of the ets-2 pointed domain decreased the interaction with BS69 in vitro. In transfection assays, co-expression of ets-2 and BS69 resulted in repression of defined ets-2 target genes. CONCLUSION: These results support a role for ets-2 as a repressor and indicate that BS69 is required as co-repressor. Phosphorylation of ets-2 may switch its activity from repressor to activator by interfering with formation of the BS69 complex.

3T3 Cells↗