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- W332994672 abstract "Background: Liver kinase B1 (LKB1), a tumor suppressor, is a central regulator of cell polarity and energy homeostasis. The roles of LKB1 in endothelial function in vivo have not been explored. Methods and Results: The endothelium-specific LKB1 knockout ( LKB1 endo -/- ) mice were generated by crossbreeding LKB1 flox/flox mice with VE-cadherin Cre approach. LKB1 endo -/- mice exhibited hypertension, cardiac hypertrophy and impaired endothelium-dependent relaxation. In addition, in parallel with reduced levels of both endothelial nitric oxidase (eNOS) activity and phosphorylated (Thr172) AMP-activated protein kinase (AMPK), a downstream enzyme of LKB1, LKB1 endo -/- mice expressed high levels of caveolin-1. Further, siRNA silencing of caveolin-1 normalized the eNOS activity in LKB1-deficient endothelial cells. Furthermore, human antigen R (HuR) bound with AU-rich elements of caveolin-1 mRNA 3’ UTR resulting in increased stability of caveolin-1 and genetic knockdown of HuR decreased caveolin-1 level in LKB1-deficient endothelial cells. Finally, we found that inhibition of LKB1 or AMPK induced the translocation of HuR from nuclei to cytosol and overexpression of constitutively active AMPK (CA-AMPK) led to decreased caveolin-1 level. Consistently, administration of CA-AMPK in LKB1 endo -/- mice lowered blood pressure with improved endothelial function in vivo . Conclusions: Our findings indicate that endothelial cell LKB1 plays an essential role in regulating eNOS activity, endothelial function, and blood pressure through modulating AMPK-mediated caveolin-1expression." @default.
- W332994672 created "2016-06-24" @default.
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- W332994672 date "2013-11-26" @default.
- W332994672 modified "2023-09-28" @default.
- W332994672 title "Abstract 10120: Endothelial Cell-specific Lkb1 Deletion Causes Endothelial Dysfunction and Hypertension in Mice In Vivo" @default.
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