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pubmed-article:12438538pubmed:abstractTextpoly(ADP-ribose) polymerase-2 (PARP-2) is a newly described member of the PARP family of nuclear enzymes. Previous studies have shown pharmacological inhibition of PARP activity to have a beneficial role in attenuating inflammation. We developed a chemically modified 2'-O-(2-methoxy)ethyl antisense oligonucleotide (ISIS 110251) inhibitor of PARP-2 and tested it for efficacy in the interleukin (IL)-10-deficient mouse. In tissue culture, ISIS 110251 reduced PARP-2 mRNA expression in a concentration- and sequence-specific manner. In 129 Sv/Ev mice, ISIS 110251 reduced PARP-2 mRNA in liver by 80%. This reduction was dependent upon treatment duration and was independent of the method of delivery. In interleukin-10-deficient mice with established colitis, treatment with ISIS 110251 normalized colonic epithelial barrier and transport function, reduced proinflammatory cytokine secretion and inducible nitric-oxide synthase activity, and attenuated inflammation. Our data demonstrate that selective inhibition of PARP-2 activity results in a marked improvement of colonic inflammatory disease in a mouse model of chronic colitis and a normalization of colonic function.lld:pubmed
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pubmed-article:12438538pubmed:statusMEDLINElld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:MoniaBrettBlld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:JijonHumberto...lld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:PopoffIanIlld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:TaverniniMich...lld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:MaMichaelMlld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:McKayRobRlld:pubmed
pubmed-article:12438538pubmed:authorpubmed-author:MadsenKarenKlld:pubmed
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pubmed-article:12438538pubmed:pagination1145-54lld:pubmed
pubmed-article:12438538pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:12438538pubmed:articleTitleAntisense oligonucleotides to poly(ADP-ribose) polymerase-2 ameliorate colitis in interleukin-10-deficient mice.lld:pubmed
pubmed-article:12438538pubmed:affiliationDivision of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada.lld:pubmed
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