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GSE32614
Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Objective: To determine the effects of age and topographic location on gene expression in human neural retina.
Publication Title
Effects of aging and anatomic location on gene expression in human retina.
Sample Metadata Fields
Sex, Age
View Samples- Rattus norvegicus
- 12 Downloadable Samples
- Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
To elucidate the fundamental molecular mechanisms responsible for multistep hepatotumorigenesis, this study investigated genes that were upregulated in a stepwise manner from the nave liver condition through to chronic oxidative stress-induced hepatitis and liver tumor by time-series microarray analysis. The time-dependent gene expression profile should reflect the multistep process of hepatotumorigenesis, and might identify genes that function specifically in hepatotumorigenesis.
Publication Title
IQGAP1 and vimentin are key regulator genes in naturally occurring hepatotumorigenesis induced by oxidative stress.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cancer cells express different sets of receptor type tyrosine kinases. These receptor kinases may be activated through autocrine or paracrine mechanisms. Fibroblasts may modify the biologic properties of surrounding cancer cells through paracrine mechansms.
Publication Title
The role of HGF/MET and FGF/FGFR in fibroblast-derived growth stimulation and lapatinib-resistance of esophageal squamous cell carcinoma.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
In order to find the difference between human lung tissue-derived fibroblasts and human vascular adventitial fibroblasts for enhancing tumor formation ablity of human lung adenocarcinoma cell line A549, we found that human vascular adventitial fibroblasts enhance A549 tumor formation in vivo compared to human lung tissue-derived fibroblasts. To find the responsible genes for this phenomena, we used microarray analysis to find the expression difference between lung tissue-derived fibroblasts and vascular adventitial fibroblas
Publication Title
Podoplanin-positive fibroblasts enhance lung adenocarcinoma tumor formation: podoplanin in fibroblast functions for tumor progression.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
We used microarrays to evaluate the effect of SRPIN803 on gene expression in ARPE-19 cells.
Publication Title
Identification of a Dual Inhibitor of SRPK1 and CK2 That Attenuates Pathological Angiogenesis of Macular Degeneration in Mice.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 36 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Glutamine supplementation suppresses herpes simplex virus reactivation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)- inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN- knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN- producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN--associated immune response and reduce the rate of reactivation of latent virus infection.
Publication Title
Glutamine supplementation suppresses herpes simplex virus reactivation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
Chronic viral infections are difficult to treat and new approaches, particularly those involving enhancing immune responses are needed. Herpes simplex virus (HSV) establishes latency, reactivates frequently, and breakthrough reactivation can occur despite suppressive antiviral therapy. Virus-specific T cells are important to control HSV, and activated T cells require increased metabolism of glutamine for their proliferation. We found that treatment of HSV-1 latently infected mice and HSV-2 infected guinea pigs with supplemental oral glutamine reduced virus reactivation. Transcriptome analysis of mice treated with glutamine showed that several interferon (IFN)- inducible genes were upregulated. Unlike wild-type mice, supplemental glutamine was ineffective in reducing the rate of HSV-1 reactivation in IFN- knock-out mice. Mice treated with glutamine had higher numbers of HSV-specific IFN- producing CD8 T cells in latently infected ganglia. Thus, glutamine may enhance the IFN--associated immune response and reduce the rate of reactivation of latent virus infection.
Publication Title
Glutamine supplementation suppresses herpes simplex virus reactivation.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Tenascin-C (TNC), a cancer-associated extracellular matrix glycoprotein, plays a pivotal role in tumor growth. To identify the genes regulated by TNC during tumor growth, we performed a tumor growth assay, DNA microarray analysis, and quantitative real-time PCR (qRT-PCR). Mouse mammary tumor cells were subcutaneously inoculated into GRS/A (WT) and GRS/A-TgH(Tnc) (TNKO) mice. Tumors in WT mice significantly increased in volume with expressing TNC while tumors in TNKO mice showed hardly detectable levels of TNC. Tumor gene expression profiles between TNKO and WT mice were compared using DNA microarray analysis. We found that 447 genes were up-regulated (TNKO>WT) and 667 genes were down-regulated (TNKO<WT) in the TNKO group. We then classified these genes by Gene Ontology (GO) terms in order to elucidate their biological function. There were three GO terms found related to tumor growth, namely, acute inflammatory response, cell adhesion, and response to wounding. Eighty-three of the genes primarily involved in these GO terms were further validated by qRT-PCR. Eight genes: Tnc, Cxcl2, Cxcl1, Hbegf, Chl1, Cd44, Serpina3n, and F3 were significantly down-regulated relative to the WT. Eighteen genes: Saa3, P2rx7, Ptgs1, Ptger2, Comp, Steap4, Il1rn, Il1b, Ncf1, Mst1, Nfb1, Ctsb, Tnfrsf1a, Tnfrsf1b, Cd24a, Adam17, Mtpn, and Sox4 were significantly up-regulated relative to the WT. These results support our hypothesis that TNC has multi-faceted effects on both the tumor cells and their microenvironment. First, TNC acts on the tumor cells directly by up-regulating genes involved in cancer cell proliferation through the CXCL1/2 and CXCR2 pathway. Second, TNC controls the tumor microenvironment by promoting angiogenesis through the CXCL1/2 and CXCR2 pathway, and by suppressing inflammatory gene expression through a separate pathway.
Publication Title
Comprehensive DNA microarray expression profiles of tumors in tenascin-C-knockout mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Dietary restriction regimens lead to enhanced stress resistance and extended lifespan in many species through the regulation of fasting and/or diet responsive mechanisms. The fasting stimulus is perceived by sensory neurons and causes behavioral and metabolic adaptations. Several studies have implicated that the nervous system is involved in the regulation of longevity. However, it remains largely unknown whether the nervous system contributes to the regulation of lifespan and/or stress resistance elicited by fasting. In this study, we first investigated the role of the nervous system in fasting-elicited longevity and stress resistance. We found that lifespan extension in Caenorhabditis elegans caused by an intermittent fasting (IF) regimen was suppressed by functional defects in sensory neurons. The IF-induced longevity was also suppressed in a mutant that lacks the enzyme required for the synthesis of an amine neurotransmitter, octopamine (OA), which acts in the absence of food, i.e., under fasting conditions. Although OA administration did not significantly extend the lifespan, it enhanced organismal resistance to oxidative stress. This enhanced resistance was suppressed by a mutation of the OA receptors, SER-3 and SER-6. Moreover, we found that OA administration promoted the nuclear translocation of DAF-16, the key transcription factor in fasting responses, and that the OA-induced enhancement of stress resistance required DAF-16. Altogether, our results suggest that OA signaling, which is triggered by the absence of food, shifts the organismal state to a more protective one to prepare for environmental stresses.
Publication Title
Octopamine enhances oxidative stress resistance through the fasting-responsive transcription factor DAF-16/FOXO in C. elegans.
Sample Metadata Fields
Specimen part
View Samples