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• W2006853487 abstract "<b><i>Background:</i></b> Phenotypic switch of vascular smooth muscle cells (VSMCs) accompanies neointima formation and associates with vascular diseases. Platelet-derived growth factor (PDGF)-induced activation of PDGFR/Akt1 and β-catenin signaling pathways in VSMCs has been implicated in vessel occlusion. Transglutaminase 2 (TG2) regulates these pathways and its levels are increased in the neointima. <b><i>Objective:</i></b> The aim of this study was to evaluate the role of TG2 in PDGF/β-catenin signaling cross-talk and assess its contribution to neointima. <b><i>Methods:</i></b> Aortic VSMCs from wild-type and TG2 knockout mice were tested in vitro for levels of VSMC markers, proliferation, migration and PDGF-induced activation of PDGFR/Akt1 and β-catenin pathways. Neointima in these mice was studied ex vivo in coronary vessels using a heart slice model and in vivo using a carotid artery ligation model. <b><i>Results:</i></b> Genetic deletion of TG2 attenuated the PDGF-induced phenotypic switch of aortic VSMCs, reduced their proliferation and migration rates, and inhibited PDGF-induced activation of PDGFR/Akt1 and β-catenin pathways in both ex vivo and in vivo neointima models. Importantly, genetic deletion of TG2 also markedly attenuated vessel occlusion. <b><i>Conclusions:</i></b> TG2 promotes neointima formation by mediating the PDGF-induced activation of the PDGFR/Akt1 and β-catenin pathways in VSMCs. This study identifies TG2 as a potential therapeutic target for blocking neointima in blood vessels." @default.
• W2006853487 created "2016-06-24" @default.
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• W2006853487 date "2014-01-01" @default.
• W2006853487 modified "2023-09-25" @default.
• W2006853487 title "Transglutaminase 2 Promotes PDGF-Mediated Activation of PDGFR/Akt1 and β-Catenin Signaling in Vascular Smooth Muscle Cells and Supports Neointima Formation" @default.
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• W2006853487 doi "https://doi.org/10.1159/000369461" @default.
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