Comment[ArrayExpressAccession]	E-GEOD-76658
MAGE-TAB Version	1.1						
Public Release Date	2016-01-08
Investigation Title	Transcriptional reprogramming and resistance to colonic mucosal injury in PARP1-deficient mice						
Comment[Submitted Name]	Transcriptional reprogramming and resistance to colonic mucosal injury in PARP1-deficient mice
Experiment Description	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.						
Term Source Name	ArrayExpress	EFO
Term Source File	http://www.ebi.ac.uk/arrayexpress/	http://www.ebi.ac.uk/efo/efo.owl					
Person Last Name	Kiela	Larmonie	Kiela				
Person First Name	Pawel	Claire	Pawel				
Person Mid Initials	R.	B	R				
Person Email	pkiela@peds.arizona.edu						
Person Affiliation	University of Arizona						
Person Phone	520-626-9687						
Person Address	Pediatrics, University of Arizona, 1501 N. Campbell Ave., Tucson, AZ, USA						
Person Roles	submitter						
Protocol Name	P-GSE76658-1	P-GSE76658-5	P-GSE76658-6	P-GSE76658-2	P-GSE76658-3	P-GSE76658-4	P-GSE76658-7
Protocol Description	The data were analyzed with GeneSpring 13.1.1, using  ExonRMA16 summarization algorithm; quantile sample normalization with baseline transformation to median of all samples ID_REF =  VALUE = normalized log signal intensity	According to menufacturer's (Affymetrix) protocol	According to menufacturer's (Affymetrix) protocol	Mice were assigned to control group (continous access to plain drinking water) or to colitis group [4% dextran sulfate sodium (DSS) for 7 days]. At sacrifice, whole colon was colected, washed, and flash-frozen in liquuid N2 for RNA isolation.	6-8 week old mice housed in conventional animal facility monitored and free of common murine pathogens (MHV, MPV, MVM, TMEV, Mycoplasma pulmonis, Sendai, EDIM, MNV, and eco- and endoparasites)	Trizol extraction of total RNA was performed according to the manufacturer's instructions, followed by column purification (Qiagen Mini RNA kit)	According to menufacturer's (Affymetrix) protocol
Protocol Type	normalization data transformation protocol	labelling protocol	hybridization protocol	sample treatment protocol	growth protocol	nucleic acid extraction protocol	array scanning protocol
Experimental Factor Name	treatment	genotype					
Experimental Factor Type	treatment	genotype					
Comment[SecondaryAccession]	GSE76658						
Comment[GEOReleaseDate]	2016-01-08						
Comment[ArrayExpressSubmissionDate]	2016-01-07						
Comment[GEOLastUpdateDate]	2016-01-10						
Comment[AEExperimentType]	transcription profiling by array						
SDRF File	E-GEOD-76658.sdrf.txt