			Home About us Contact

Used cDNA Microarrays (used + cdna_microarray)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Highly conserved gene expression profiles in humans with allergic rhinitis altered by immunotherapy

CLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2005
Z. Liu
Summary Background Atopic diseases, resulting from hypersensitivity to a wide variety of allergens, affect 10,20% of the population. Immunotherapy is an effective treatment for atopic diseases, but its mechanisms are not fully understood. Objective We studied gene expression profiles in the peripheral blood mononuclear cells (PBMC) and examined whether the individuals with allergic rhinitis (AR) have a unique gene expression profile and how the immunotherapy affect the gene expression profiles. Methods We used cDNA microarray and ,expression analysis systemic explorer' to examine the gene expression profiles in the PBMC of atopic subjects and other groups. Results We identified a highly conserved gene expression profile in atopic subjects that permitted their accurate segregation from control or autoimmune subjects. A major feature of this profile was the under-expression of a variety of genes that encode proteins required for apoptosis and over-expression of genes that encode proteins critical for stress responses and signal transduction. We also identified 563 genes that can segregate individuals with AR based upon receipt of immunotherapy. Conclusion There is a highly conserved gene expression profile in the PBMC of individuals with AR. This profile can be used to identify individuals with AR and to evaluate responses to immunotherapy. Quantitative endpoints, such as gene expression, may assist clinicians faced with clinical decisions in the diagnosis of patients and the evaluation of response to therapy. The knowledge of the possible genetic basis for immunotherapy efficacy may also lead to novel therapeutic approaches for atopic diseases. [source]

Analysis of gene expression profiles in human HL-60 cell exposed to cantharidin using cDNA microarray

INTERNATIONAL JOURNAL OF CANCER, Issue 2 2004
Jun-Ping Zhang
Abstract Cantharidin is a natural toxin that has antitumor properties and causes leukocytosis as well as increasing sensitivity of tumor cells resistant to other chemotherapeutic agents. There is limited information, however, on the molecular pharmacological mechanisms of cantharidin on human cancer cells. We have used cDNA microarrays to identify gene expression changes in HL-60 promyeloid leukemia cells exposed to cantharidin. Cantharidin-treated cells not only decreased expression of genes coding for proteins involved in DNA replication (e.g., DNA polymerase delta), DNA repair (e.g., FANCG, ERCC), energy metabolism (e.g., isocitrate dehydrogenase alpha, ADP/ATP translocase), but also decreased expression of genes coding for proteins that have oncogenic activity (e.g., c-myc, GTPase) or show tumor-specific expression (e.g., phosphatidylinositol 3-kinase). In contrast, these treated cells overexpressed several genes that encode intracellular and secreted growth-inhibitory proteins (e.g., BTG2, MCP-3) as well as proapoptotic genes (e.g., ATL-derived PMA-responsive peptide). Our findings suggest that alterations in specific genes functionally related to cell proliferation or apoptosis may be responsible for cantharidin-mediated cytotoxicity. We also found that exposure of HL-60 cells to cantharidin resulted in the decreased expression of multidrug resistance-associated protein genes (e.g., ABCA3, MOAT-B), suggesting that cantharidin may be used as an oncotherapy sensitizer, and the increased expression of genes in modulating cytokine production and inflammatory response (e.g., NFIL-3, N-formylpeptide receptor), which may partly explain the stimulating effects on leukocytosis. Our data provide new insight into the molecular mechanisms of cantharidin. © 2003 Wiley-Liss, Inc. [source]

Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 17

JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003
M Scarlato
The neuropilins, NP-1 and NP-2, are co-receptors for Sema3A and Sema3F, respectively, both of which are repulsive axonal guidance molecules. NP-1 and NP-2 are also co-receptors for vascular endothelial growth factor (VEGF). The neuropilins and their ligands are known to play prominent roles in axonal pathfinding, fasciculation, and blood vessel formation during peripheral nervous system (PNS) development. To screen for additional molecular mechanisms by which Schwann cells and fibroblasts contribute to successful PNS axonal regeneration, we used cDNA microarrays (Clontech) to compare expression profile of multiple messenger RNAs in sciatic nerves distal to transection with their levels in normal sciatic nerves. An evocative result of this screen was a 14-fold increase in NP-2 mRNA in the axotomized nerve segments 4 days post-transection. We verified that NP-2 is induced in transected as well as crushed nerve segments by quantitative PCR, Northern blotting, and Western blotting, and examined the distribution of NP-2 expressing cells in injured sciatic nerves by in situ hybridization. Then, we sought evidences of induction in the injured nerves of the NP-2 ligands, Sema3F and VEGF, and widened our survey to determine whether expression of the functionally related genes, neuropilin-1 (NP-1) and its class 3 semaphorin ligand, Sema3A are also induced in PNS following injury. We showed by in situ hybridization induction of all those genes at four days post-crushed, distally to the lesion. Our results suggest the possibility that the neuropilins and their semaphorin ligands serve to guide, rather than to impede, regenerating axons in the adult PNS. [source]

Gene Expression during Formation of Earlywood and Latewood in Loblolly Pine: Expression Profiles of 350 Genes

PLANT BIOLOGY, Issue 6 2004
U. Egertsdotter
Abstract: The natural variability of wood formation in trees affords opportunities to correlate transcript profiles with the resulting wood properties. We have used cDNA microarrays to study transcript abundance in developing secondary xylem of loblolly pine (Pinus taeda) over a growing season. The cDNAs were selected from a collection of 75 000 ESTs that have been sequenced and annotated (http:web.ahc.umn.edubiodatansfpine). Cell wall thickness and climatic data were related to earlywood and latewood formation at different time points during the growing season. Seventy-one ESTs showed preferential expression in earlywood or latewood, including 23 genes with no significant similarity to genes in GenBank. Seven genes involved in lignin synthesis were preferentially expressed in latewood. The studies have provided initial insights into the variation of expression patterns of some of the genes related to the wood formation process. [source]

YB-1 is upregulated during prostate cancer tumor progression and increases P-glycoprotein activity

THE PROSTATE, Issue 3 2004
Pepita Giménez-Bonafé
Abstract BACKGROUND Currently, the main obstacle to curing advanced prostate cancer is development of androgen independence (AI), where malignant cells acquire the ability to survive in the absence of androgens. Our initial experimental approach used cDNA microarrays to characterize changes in gene expression in the LNCaP human prostate tumor model during progression to AI. The transcription factor Y-box binding protein (YB-1) was shown to be one of the genes upregulated. We focused on increased YB-1 expression during progression in clinical specimens, and further examined one of its downstream targets, P-glycoprotein (P-gp). METHODS Northern blot analysis was performed on LNCaP tumor series, as well as immunohistochemical analyses of human prostate cancer tissue samples. YB-1 was transiently transfected and transport analysis were performed to analyze P-gp efflux activity. RESULTS YB-1 expression is markedly increased during benign to malignant transformation and further following androgen ablation. In addition, increased YB-1 expression after castration in the LNCaP model is linked to upregulation of P-gp. We demonstrate that YB-1 upregulates P-gp activity resulting in a 40% intracellular decrease in the P-gp substrate vinblastine. We have also found that P-gp increases the efflux of the endogenous androgen, dihydrotestosterone (DHT), from prostate cells and leads to decreased androgen regulated gene expression. CONCLUSIONS We hypothesize that early in prostate cancer progression, increased expression of YB-1 may increase P-gp activity which may in turn lower androgen levels in the prostate tumor cells. Suppression of androgen levels may activate cell survival pathways and lead to an adaptive survival advantage of androgen independent prostate cancer cells following androgen ablation therapy. © 2004 Wiley-Liss, Inc. [source]