Transcription profiling of human entorhinal cortex cells from suicide patients with major depression.
ABSTRACT: RNAs were extracted from entorhinal cortex of human suicide patients with major depression and matched control subjects. The transcription profile was investigated by Agilent microarray platform and quantitative real-time PCR to reveal alterations in neuronal functions in this brain region.
Project description:Total RNAs were extracted from the hippocampus and prefrontal cortex of anxious mice. The transcriptome of the two brain regions were investigated using a custom made Agilent 8 x 15k features oligo microarray.
Project description:We observed extensive neurite formation in NG108-15 cells cultured in the presence of the flavonoid, isoquercitrin. To help determine the mechanism of neuritogenesis, microarray analysis was performed on samples treated with 40 uM isoquercitrin for 24 hrs.
Project description:The well-known colorectal adenoma-carcinoma sequence suggests that a normal epithelial cell, through accumulations of genetic lesion and epigenetic disregulation can transform into a benign adenoma then further develop into a cancer. Using microarray-based comparative genomic hybridization (CGH), we reveal genome-wide copy number variations in colorectal cancer and polyp and use them to determine the tissues clonal relationship.
Project description:G. max plants was grown in plastic pots filled with soil for 3 weeks under a 12 h light/12 h dark at 28°C. Cold treatment: The 3-week-old plants were transferred from 28°C to 4°C and were grown for 1 day. Dehydration treatment: The 3-week-old plants were grown for 4 days without watering.
Project description:Epidemiologic studies have shown a significant inverse correlation between fruit and vegetable consumption and incidence of esophageal adenocarcinoma. Procyanidins are polymeric flavanols found in many fruits and vegetables, and have been shown to possess anti-carcinogenic/chemopreventive properties. We previously showed that an oligomeric procyanidin extracted from apples with an average degree of polymerisation of 3.9 induced cell cycle arrest and apoptosis in the esophageal adenocarcinoma cell line OE33. In order to understand the mechanism of action of this procyanidin we determined genome-wide transcriptomic changes induced by procyanidin treatment of OE33 cells. Pathway analysis of these data implicated the MAP kinase signalling pathways in eliciting these responses. An investigation into the role of these pathways showed that procyanidin specifically induced the activation of the stress-activated protein (SAP) kinases JNK1/2 and p38-? and ? leading to the increased expression of JUN and the phosphatases DUSP1 and -10. Gene-specific knockdown of the expression of JNK1, JNK2, p38-?, p38-? or JUN diminished procyanidin-induced effects on apoptosis demonstrating a clear role for these pathways. JUN is a component of the transcription factor AP-1 and AP-1 binding sites are over-represented in the promoters of procyanidin-induced genes, which together with the demonstration that JUN occupies several such promoters highlight the importance of this transcription factor in mediating the cellular response to procyanidin. These data provide a mechanistic understanding of how procyanidin specifically targets distinct pathways involved in the induction of apoptosis in esophageal adenocarcinoma cells and will inform future studies investigating its use as a chemopreventive/therapeutic agent.