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Glycogen synthase kinase 3-? inhibition induces lymphangiogenesis through ?-catenin-dependent and mTOR-independent pathways.

ABSTRACT: Lymphatic vessels play an important role in health and in disease. In this study, we evaluated the effects of GSK3-? inhibition on lung lymphatic endothelial cells in vitro. Pharmacological inhibition and silencing of GSK3-? resulted in increased lymphangiogenesis of lung lymphatic endothelial cells. To investigate mechanisms of GSK3-?-mediated lymphangiogenesis, we interrogated the mammalian/mechanistic target of rapamycin pathway and found that inhibition of GSK3-? resulted in PTEN activation and subsequent decreased activation of AKT, leading to decreased p-P70S6kinase levels, indicating inhibition of the mTOR pathway. In addition, consistent with a negative role of GSK3-? in ?-catenin stability through protein phosphorylation, we found that GSK3-? inhibition resulted in an increase in ?-catenin levels. Simultaneous silencing of ?-catenin and inhibition of GSK3-? demonstrated that ?-catenin is required for GSK3-?-induced lymphangiogenesis.

SUBMITTER: Stump B 

PROVIDER: S-EPMC6456176 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Glycogen synthase kinase 3-β inhibition induces lymphangiogenesis through β-catenin-dependent and mTOR-independent pathways.

Stump Benjamin B   Shrestha Shikshya S   Lamattina Anthony M AM   Louis Pierce H PH   Cho Woohyun W   Perrella Mark A MA   Ai Xingbin X   Rosas Ivan O IO   Wagner Florence F FF   Priolo Carmen C   Astin Jonathan J   El-Chemaly Souheil S  

PloS one 20190409 4

Lymphatic vessels play an important role in health and in disease. In this study, we evaluated the effects of GSK3-β inhibition on lung lymphatic endothelial cells in vitro. Pharmacological inhibition and silencing of GSK3-β resulted in increased lymphangiogenesis of lung lymphatic endothelial cells. To investigate mechanisms of GSK3-β-mediated lymphangiogenesis, we interrogated the mammalian/mechanistic target of rapamycin pathway and found that inhibition of GSK3-β resulted in PTEN activation  ...[more]

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