Project description:Inflammatory bowel disease (IBD) is one of the intractable diseases. Nutritional components associated with IBD have been identified, and it is known that excessive methionine intake exacerbates inflammation and that tryptophan metabolism is involved in inflammation. In this study, we examined how temporary methionine, tryptophan, and niacin deficiencies alter gene expression in the intestinal cells of a dextran sulfate sodium (DSS)-fed IBD mouse model. The results showed that feeding amino acid deficient diets increased the expression of serine proteases and fat metabolizing enzymes. Amino acid deficiency also activated one-carbon metabolism and the PPAR pathway. These results suggest that temporary amino acid deficiency may be useful to enhance the antioxidant activity of the host.
Project description:Differential gene expression to parasite and nonparasite antigen was seen in infected patients with lifelong exposure to the human filarial parasite Loa loa (endemics) compared with patients who became infected due to temporary residence or travel in an endemic country (expatriates).
Project description:We sought to assess how temporary loss of the microtubule-associated protein CRMP2A could affect global gene expression in the A549 lung cancer cells. We used microarrays to identify differentially regulated genes when CRMP2A is temporarily removed from A549 cells using siRNA.
Project description:A rat model of acute mitochondrial dysfunction in the cochlea is created by applying an irreversible mitochondrial complex II enzyme inhibitor, 3-NP, directly to the round window membrane. Treatment with 300 mM 3-NP results in temporary hearing loss (temporary threshold shift (TTS) model), whereas treatment with 500 mM 3-NP results in profound and permanent hearing loss (permanent threshold shift (PTS) model. Either treatment results with a primary histological change in the lateral wall spiral ligament. Because local ATP deprivation in the inner ear results from inhibition of inner ear mitochondrial function, this model replicates the etiology of inner ear energy failure caused by ATP deprivation due to inner ear ischemia. We used microarrays to detail the global programme of gene expression in the damaged cochlear lateral wall by 3NP and identified distinct classes of up-regulated/ down-regulated genes during the process. One and three day after administrated either 300 mM of 3-NP (TTS-1d and TTS-3d, respectably) or saline (Ctrl-1d and Ctrl-3d, respectably), rat cochear lateral wall in the apical side of the basal turn was harvested for RNA extraction and hybridization on Affymetrix microarrays.
Project description:The transcriptional mechanisms by which temporary exposure to developmental signals instigates adipocyte differentiation are unknown. During early adipogenesis, we find transient enrichment of the glucocorticoid receptor (GR), CCAAT/enhancer binding protein b (CEBPb), p300, mediator subunit 1, and histone H3 acetylation near genes involved in cell proliferation, development and differentiation, including the gene encoding the master regulator of adipocyte differentiation, peroxisome proliferator activated receptor g2 (PPARg2). Occupancy and enhancer function are triggered by adipogenic signals, and diminish upon their removal. GR, which is required for adipogenesis but need not be active in the mature adipocyte, transiently functions with other enhancer proteins to propagate a new program of gene expression that includes induction of PPARg2, thereby providing a memory of the earlier adipogenic signal. Thus, the conversion of preadipocyte to adipocytes involves the formation of an epigenomic transition state that is not observed in cells at the beginning or end of the differentiation process. Genomic occupancy profiled by high throughput sequencing (ChIP-seq) from 3T3-L1 cells during differentiation for H3K9Ac, CEBPb and GR.
Project description:Somatic cells acclimate to changes in the environment by temporary reprogramming. Much has been learned about transcription factors that induce these cell-state switches in both plants and animals, but how cells rapidly modulate their proteome remains elusive. Here, we show rapid induction of autophagy during temporary reprogramming in plants triggered by phytohormones, immune and danger signals. Quantitative proteomics following sequential reprogramming revealed that autophagy is required for timely decay of previous cellular states and for tweaking the proteome to acclimate to the new conditions. Signatures of previous cellular programs thus persist in autophagy deficient cells, affecting cellular decision-making. Concordantly, autophagy deficient cells fail to acclimatize to dynamic climate changes. Similarly, they have defects in dedifferentiating into pluripotent stem cells, and redifferentiation during organogenesis. These observations indicate that autophagy mediates cell state switches that underlie somatic cell reprogramming in plants and possibly other organisms, and thereby promotes phenotypic plasticity.
Project description:Because most human stroke victims are elderly, studies of experimental stroke in the aged rather than the young rat model may be optimal for identifying clinically relevant cellular responses, as well for pinpointing beneficial interventions. We employed the Affymetrix platform to analyze the whole-gene transcriptome following temporary ligation of the middle cerebral artery in aged and young rats. Expression profiling of periinfarcted brain areas of young and aged rats, as well as healthy tissue from naive animals.
Project description:Differential gene expression to parasite and nonparasite antigen was seen in infected patients with lifelong exposure to the human filarial parasite Loa loa (endemics) compared with patients who became infected due to temporary residence or travel in an endemic country (expatriates). CD4+ and CD8+ cells were isolated; comparison was done between unstimulated cells from 2 patient groups and between parasite microfilarial (MfAg) and nonparasite streptolysin O (SLO) antigen-stimulated cells with unstimulated cells; Technical replicates (2 unstimulated; 2 each antigen)