Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse macrophage response to sendai virus infection.

ABSTRACT: Thus, mouse macrophage cultures were established from PBMCs isolated from wild-type control mice and were inoculated with SeV (Sendai virus) or UV-SeV (UV-inactivated SeV). These microarrays were performed in concert with assays of CCL5 and CCR5 expression, viral replication, and cellular apoptosis. Initial experiments indicated that wild-type mouse macrophages inoculated with SeV exhibit induction of CCL5 mRNA to the highest level of any known mouse gene product, while mRNA levels for CCL5 receptors (CCR5 as well as CCR3 and CCR1) or alternative ligands for these receptors (CCL3 and CCL4) were relatively unchanged by viral infection. Experiment Overall Design: Macrophages were pooled from mice and subsequently cultured (~3 mice/well). Each culture well was then subjected to one of two treatments (SeV, or UV-SeV) for 4 days. Thus, per condition, N = 2 culture wells, with each well independently analyzed by microarray. No technical replicates were performed, but arrays were evaluated for quality control using the SimpleAffy package (Miller CJ, 2004) in Bioconductor 1.5.

ORGANISM(S): Mus musculus

SUBMITTER: Anand Champak Patel

PROVIDER: E-GEOD-2935 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection.

Tyner Jeffrey W JW Uchida Osamu O Kajiwara Naohiro N Kim Edy Y EY Patel Anand C AC O'Sullivan Mary P MP Walter Michael J MJ Schwendener Reto A RA Cook Donald N DN Danoff Theodore M TM Holtzman Michael J MJ

Nature medicine 20051002 11

Host defense against viruses probably depends on targeted death of infected host cells and then clearance of cellular corpses by macrophages. For this process to be effective, the macrophage must presumably avoid its own virus-induced death. Here we identify one such mechanism. We show that mice lacking the chemokine Ccl5 are immune compromised to the point of delayed viral clearance, excessive airway inflammation and respiratory death after mouse parainfluenza or human influenza virus infection ...[more]

PMID: 16208318

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Project description:In patients with severe kidney disease AVF are surgically placed in order to create good access for hemodialysis. In these dialysis patients the failure rates of AVF can be as high as 24% within 6 months after surgery, causing ineffective dialysis and necessitating additional clinical interventions. The pathological processes known to lead to AVF failure are beginning to be unravelled include the formation of venous neointimal hyperplasia (VNIH), thrombosis (Chang et al. PMID 16105066), and venous stenosis (Kanterman et al. PMID7892454, Tang et al. 1998), resulting in a reduced blood flow through the fistula. We established a rat model for AVF failure in human kidney dialysis patients. The characterization of this model has been previously described (Globerman et al. 2011, PubmedID:22002501). In this model the AVFs are surgically constructed in the right leg by connecting the superficial epigastric vein SEV to the common femoral artery (CFA), resulting in exposure of the SEV to arterial pressure with pulsatile and low resistant flow patterns (Globerman et al. 2011, PMID22002501). In the present study we utilized this AVF model in order to assess the effects of arterialized flow, with consequent pathological changes of the vessel wall due to surgical AVF instalment, on the transcriptome of endothelium from the SEV. Within the SEV these pathologies of the vessel wall include the formation of NIH in the main branch, and stenosis in the side branches. By employing this rat model we assessed the changes of the endothelial transcriptome in relation to these pathologies in order to gain mechanistic understanding of the potential roles of venous endothelium in AVF failure, as well as to identify potential biomarkers preceding AVF failure. AVF surgery was performed on N=6 rats, and 13-14 days after surgery the rats were sacrificed. AVFs were extracted from the rats, and microarray transcriptome analyses were performed on luminal endothelial cells that isolated from four different sites of the AVF by employing Laser Capture Microdissection (LCM). These sites included (i) N=5 AVF sections of the superficial epigastric vein (SEV) with neointimal hyperplasia (NIH), (ii) N=3 AVF sections of SEV side branches with luminal stenosis, (iii), N=6 sections of the SEV located distally from a ligation thereby omitting exposure to arterialized flow and consequently preventing the development of NIH or stenosis, and (iv) N=3 sections of the AVF common femoral artery without signs of NIH or stenosis.

Dataset Information

Transcription profiling of mouse macrophage response to sendai virus infection.

Publications

CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection.

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