LKB1 deficiency in Tie2-Cre-expressing cells impairs ischemia-induced angiogenesis.

ABSTRACT: LKB1 is a tumor suppressor protein whose loss leads to HIF1alpha-mediated activation of a proangiogenic program in intestinal polyps. LKB1 is also protein kinase regulator of AMP-activated protein kinase (AMPK) signaling, which is essential for endothelial cell responses to tissue ischemia. To discern whether LKB1 signaling is either pro- or antiangiogenic, we investigated ischemia-induced revascularization in mice that were deficient for LKB1 in Tie2-Cre-expressing cells. Whereas homozygous deletion of LKB1 led to embryonic lethality, heterozygous LKB1-knock-out (KO) (Lkb1(flox/+);Tie2(Tg/+)) mice were viable. Unchallenged heterozygous LKB1-KO mice displayed normal capillary density, but the revascularization of hind limb following ischemic surgery was significantly impaired as evaluated

SUBMITTER: Ohashi K 

PROVIDER: S-EPMC2903404 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature