DNA microarray analyses reveal a post-irradiation differential time-dependent gene expression profile in yeast cells exposed to X-rays and γ-rays

2006 ◽  
Vol 346 (1) ◽  
pp. 51-60 ◽  
Author(s):  
Shinzo Kimura ◽  
Emi Ishidou ◽  
Sakiko Kurita ◽  
Yoshiteru Suzuki ◽  
Junko Shibato ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Dna Microarray ◽  
Expression Profile ◽  
Time Dependent ◽  
Yeast Cells ◽  
X Rays ◽  
Post Irradiation ◽  
Γ Rays ◽  
Microarray Analyses

Novel Stratification Scheme for AML Based on a Large-Scale DNA Microarray Analysis of CD133-Positive Blasts.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2043-2043
Author(s):  
Hiroyuki Mano ◽  
Yoshihiro Yamashita
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Microarray Analysis ◽  
Dna Microarray ◽  
Expression Profile ◽  
Treatment Strategy ◽  
Large Scale ◽  
Dna Microarray Analysis ◽  
Wide Range ◽  
Microarray Analyses

Abstract AML is a clonal disorder of immature hematopoietic blasts and has a variable clinical outcome. Current classification of AML is based predominantly on the cytogenetic abnormalities and morphology of the malignant blasts and is not always helpful for optimization of treatment strategy. It is, for instance, very difficult to predict the prognosis of AML patients with a normal karyotype, who constitute ~50% of the AML population. DNA microarray analysis has the potential to provide a novel stratification scheme for AML patients, which is based on gene expression profile, and might help to predict the prognosis of, and optimize the treatment strategy for, each affected individual. However, leukemic blasts derived from bone marrow (BM) of AML-related disorders, are not homogeneous. The blasts may constitute from 20% to almost 100% of mononuclear cells (MNCs) in the marrow. Furthermore, given that many leukemic blasts possess the ability to differentiate to a certain extent, the marrow of AML patients contains not only the immature blasts (leukemic stem clone) but also differentiated blasts. A simple comparison of BM MNCs among heterogeneous AML patients is thus likely to reveal a large number of changes in gene expression that only reflect differences either in the percentage of blasts or in the differentiation ability of the blasts. To minimize such population-shift effects in microarray analyses, we established a large-scale cell depository “Blast Bank” for the storage of CD133 (AC133)-positive hematopoietic stem cell-like fractions from individuals with a wide range of hematopoietic disorders. In the present study, we have used Affymetrix HGU133 A&B microarrays to measure the expression profiles of ~33,000 genes in the Blast Bank specimens of 99 adults with AML-related disorders: 83 individuals with AML and 16 patients in the RAEB stage of MDS. In contrast to the previous microarray analyses of BM MNCs of AML, unsupervised hierarchical clustering of the subjects based on the expression profile did not separate the patients into FAB subtype-matched subgroups. Comparison of gene expression profile between the long-time and short-time survivors has identified a small number of outcome-related genes. Supervised class prediction, based on these genes, with k-nearest neighbor method or Cox proportional hazard model both succeeded to clearly separate individuals into subgroups with statistically distinct prognoses. Our analysis may pave a way toward the expression profile-based novel stratification scheme for AML.

scholarly journals Effect of agonal and postmortem factors on gene expression profile: quality control in microarray analyses of postmortem human brain

2004 ◽  
Vol 55 (4) ◽  
pp. 346-352 ◽  
Author(s):  
Hiroaki Tomita ◽  
Marquis P Vawter ◽  
David M Walsh ◽  
Simon J Evans ◽  
Prabhakara V Choudary ◽  
...  
Keyword(s):  
Gene Expression ◽  
Quality Control ◽  
Human Brain ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Postmortem Human Brain ◽  
Microarray Analyses

scholarly journals Gene Expression Profiling of Leiomyoma and Myometrial Smooth Muscle Cells in Response to Transforming Growth Factor-β

Endocrinology ◽  
2005 ◽  
Vol 146 (3) ◽  
pp. 1097-1118 ◽  
Author(s):  
Xiaoping Luo ◽  
Li Ding ◽  
Jingxia Xu ◽  
Nasser Chegini
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Binding Protein ◽  
Muscle Cells ◽  
Time Dependent ◽  
Early Gene ◽  
A Cell

Altered expression of the TGF-β system is recognized to play a central role in various fibrotic disorders, including leiomyoma. In this study we performed microarray analysis to characterize the gene expression profile of leiomyoma and matched myometrial smooth muscle cells (LSMC and MSMC, respectively) in response to the time-dependent action of TGF-β and, after pretreatment with TGF-β type II receptor (TGF-βRII) antisense oligomer-blocking/reducing TGF-β autocrine/paracrine actions. Unsupervised and supervised assessments of the gene expression values with a false discovery rate selected at P ≤ 0.001 identified 310 genes as differentially expressed and regulated in LSMC and MSMC in a cell- and time-dependent manner by TGF-β. Pretreatment with TGF-βRII antisense resulted in changes in the expression of many of the 310 genes regulated by TGF-β, with 54 genes displaying a response to TGF-β treatment. Comparative analysis of the gene expression profile in TGF-βRII antisense- and GnRH analog-treated cells indicated that these treatments target the expression of 222 genes in a cell-specific manner. Gene ontology assigned these genes functions as cell cycle regulators, transcription factors, signal transducers, tissue turnover, and apoptosis. We validated the expression and TGF-β time-dependent regulation of IL-11, TGF-β-induced factor, TGF-β-inducible early gene response, early growth response 3, CITED2 (cAMP response element binding protein-binding protein/p300-interacting transactivator with ED-rich tail), Nur77, Runx1, Runx2, p27, p57, growth arrest-specific 1, and G protein-coupled receptor kinase 5 in LSMC and MSMC using real-time PCR. Together, the results provide the first comprehensive assessment of the LSMC and MSMC molecular environment targeted by autocrine/paracrine action of TGF-β, highlighting potential involvement of specific genes whose products may influence the outcome of leiomyoma growth and fibrotic characteristics by regulating inflammatory response, cell growth, apoptosis, and tissue remodeling.

scholarly journals Gene expression profile analysis of genes in rat hippocampus from antidepressant treated rats using DNA microarray

2010 ◽  
Vol 11 (1) ◽  
pp. 152 ◽  
Author(s):  
Jun-Ho Lee ◽  
Eunjung Ko ◽  
Young-Eun Kim ◽  
Ji-Young Min ◽  
Jian Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Dna Microarray ◽  
Expression Profile ◽  
Profile Analysis ◽  
Rat Hippocampus ◽  
Expression Profile Analysis

scholarly journals Blood Genomic Expression Profile for Neuronal Injury

2003 ◽  
Vol 23 (3) ◽  
pp. 310-319 ◽  
Author(s):  
Yang Tang ◽  
Alex C. Nee ◽  
Aigang Lu ◽  
Ruiqiong Ran ◽  
Frank R. Sharp
Keyword(s):  
Gene Expression ◽  
Brain Injury ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Whole Blood ◽  
Neuronal Injury ◽  
Adult Rats ◽  
Mild Brain Injury ◽  
Microarray Analyses ◽  
Genomic Response

This study determined whether stroke and other types of insults produced a gene expression profile in blood that correlated with the presence of neuronal injury. Adult rats were subjected to ischemic stroke, intracerebral hemorrhage, status epilepticus, and insulin-induced hypoglycemia and compared with untouched, sham surgery, and hypoxia animals that had no brain injury. One day later, microarray analyses showed that 117 genes were upregulated and 80 genes were downregulated in mononuclear blood cells of the “injury” (n = 12) compared with the “no injury” (n = 9) animals. A second experiment examined the whole blood genomic response of adult rats after global ischemia and kainate seizures. Animals with no brain injury were compared with those with brain injury documented by TUNEL and PANT staining. One day later, microarray analyses showed that 37 genes were upregulated and 67 genes were downregulated in whole blood of the injury (n = 4) animals compared with the no-injury (n = 4) animals. Quantitative reverse transcription–polymerase chain reaction confirmed that the vesicular monoamine transporter-2 increased 2.3- and 1.6-fold in animals with severe and mild brain injury, respectively, compared with no-injury animals. Vascular tyrosine phosphatase-1 increased 2.0-fold after severe injury compared with no injury. The data support the hypothesis that there is a peripheral blood genomic response to neuronal injury, and that this blood response is associated with a specific blood mRNA gene expression profile that can be used as a marker of the neuronal damage.

Microarray analyses of the effects of NF-κB or PI3K pathway inhibitors on the LPS-induced gene expression profile in RAW264.7 cells

2009 ◽  
Vol 21 (7) ◽  
pp. 1109-1122 ◽  
Author(s):  
Sofia Dos Santos Mendes ◽  
Aurélie Candi ◽  
Martine Vansteenbrugge ◽  
Marie-Rose Pignon ◽  
Hidde Bult ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Pi3k Pathway ◽  
Raw264.7 Cells ◽  
Microarray Analyses

Large-scale reprogramming of cranial neural crest gene expression by retinoic acid exposure

2004 ◽  
Vol 19 (2) ◽  
pp. 184-197 ◽  
Author(s):  
Sarah S. Williams ◽  
John P. Mear ◽  
Hung-Chi Liang ◽  
S. Steven Potter ◽  
Bruce J. Aronow ◽  
...  
Keyword(s):  
Gene Expression ◽  
Retinoic Acid ◽  
Neural Crest ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Function Analysis ◽  
Active Form ◽  
Time Dependent ◽  
Cranial Neural Crest ◽  
Increased Risk

Although retinoic acid (RA), the active form of vitamin A, is required for normal embryonic growth and development, it is also a powerful teratogen. Infants born to mothers exposed to retinoids during pregnancy have a 25-fold increased risk for malformations, nearly exclusively of cranial neural crest-derived tissues. To characterize neural crest cell responses to RA, we exposed murine crest cultures to teratogenic levels of RA and subjected their RNA to microarray-based gene expression profile analysis using Affymetrix MG-U74Av2 GeneChips. RNAs were isolated from independent cultures treated with 10−6 M RA for 6, 12, 24, or 48 h. Statistical analyses of gene expression profile data facilitated identification of the 205 top-ranked differentially regulated genes whose expression was reproducibly changed by RA over time. Cluster analyses of these genes across the independently treated sample series revealed distinctive kinetic patterns of altered gene expression. The largest group was transiently affected within the first 6 h of exposure, representing early responding genes. Group 2 showed sustained induction by RA over all times, whereas group 3 was characterized by the suppression of a time-dependent expression increase normally seen in untreated cells. Additional patterns demonstrated time-dependent increased or decreased expression among genes not normally regulated to a significant extent. Gene function analysis revealed that more than one-third of all RA-regulated genes were associated with developmental regulation, including both canonical and noncanonical Wnt signaling pathways. Multiple genes associated with cell adhesion and cell cycle regulation, recognized targets for the biological effects of RA, were also affected. Taken together, these results support the hypothesis that the teratogenic effects of RA derive from reprogramming gene expression of a host of genes, which play critical roles during embryonic development regulating pathways that determine subsequent differentiation of cranial neural crest cells.

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