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E-GEOD-76658 - Transcriptional reprogramming and resistance to colonic mucosal injury in PARP1-deficient mice

Released on 8 January 2016, last updated on 25 January 2016
Mus musculus
Samples (12)
Array (1)
Protocols (7)
Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate, and participate to the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator - cytokines, chemokines and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to determine the impact of Parp1 deletion on the innate immune response to mucosal injury. Genome-wide analysis of the colonic transcriptome was performed. Compared to WT, we demonstrated that Parp1-/-were protected from DSS-induced colitis and that this protection was associated with a dramatic transcriptional reprogramming in the colon. WT or Parp1-/- mice were treated with drinking water administered ad libitum without ot with 4% dextran sulfate (DSS) for seven days. Whole colon was collected for RNA extraction and hybridization on Affymetrix microarrays. Thee mice from each genotype/treatment groups were used in the analysis.
Experiment type
transcription profiling by array 
Pawel R. Kiela <>, Claire B Larmonie, Pawel R Kiela
Investigation descriptionE-GEOD-76658.idf.txt
Sample and data relationshipE-GEOD-76658.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-GEOD-16570.adf.txt