MARC Record from University of Toronto

LEADER: 02177nam 2200241 4500
001 AAIMR07488
005 20060407065155.5
008 060407s2005 onc|||||||||||||| ||eng d
020 $a0494074884
039 $fws
100 1 $aBan, Kiwon.
245 14 $aThe role of phosphatidylinositol-3 kinase isomers in myocardial ischemic preconditioning.
260 $c2005.
300 $a113 leaves.
500 $aSource: Masters Abstracts International, Volume: 44-02, page: 0732.
502 $aThesis (M.Sc.)--University of Toronto, 2005.
506 $aElectronic version licensed for access by U. of T. users.
520 $aIschemic preconditioning (IPC) is a novel cell protection mechanism whereby brief periods of sublethal ischemia can protect the myocyte from prolonged ischemia-induced-injury. Recently, several papers suggested that phosphatidylinositol-3 kinase (PI3K) plays an important role in IPC protection. Our study examined the isoform specificity of PI3K in IPC using PI3Kgamma knockout (PI3Kgamma-/-) and PI3Kalpha dominant-negative (PI3KalphaDN) mice. Recovery rate in IPC group was significantly higher than I/R group in wild type hearts. However, the protective effect of IPC was completely abolished in PI3Kgamma-/- hearts. Surprisingly, PI3KalphaDN hearts showed significant recovery after both I/R and IPC. Therefore our studies suggested that PI3Kgamma isomer is involved in IPC and genetic inhibition of PI3Kalpha is resistant against ischemia. Furthermore, examining downstream of PI3K revealed that PI3Kgamma-PKB/Akt-GSK3beta signaling cascade is critical for regulating cell survival. Selective inhibition PI3Kalpha or activation of PI3Kalpha may be novel therapeutic strategies for protecting the ischemic myocardium.
590 $aGERSTEIN MICROTEXT copy on microfiche (2 microfiches).
653 $aBiology, Animal Physiology.
856 41 $uhttp://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=370454&T=F$yConnect to resource
949 $aOnline resource 370454$wASIS$c1$i5859670-2001$lONLINE$mE_RESOURCE$rY$sY$tE_RESOURCE$u1/5/2006
949 $atheses masters$wALPHANUM$c1$i31761069144871$lMICROTEXT$mMEDIA_COMM$rY$sY$tMICROFORM$u1/5/2006$o.PUBLIC.