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      Triiodothyronine Potentiates Vasorelaxation via PKG/VASP Signaling in Vascular Smooth Muscle Cells.

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          Abstract

          Vascular relaxation caused by Triiodothyronine (T3) involves direct activation of endothelial cells (EC) and vascular smooth muscle cells (VSMC). Activation of protein kinase G (PKG) has risen as a novel contributor to the vasorelaxation mechanism triggered by numerous stimuli. We hypothesize that T3-induced vasorelaxation involves PKG/vasodilator-stimulated phosphoprotein (VASP) signaling pathway in VSMC.

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          Author and article information

          Journal
          Cell Physiol Biochem
          Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
          S. Karger AG
          1421-9778
          1015-8987
          2017
          : 41
          : 5
          Affiliations
          [1 ] Department of Life Sciences, New York Institute of Technology, Old Westbury, New York, New York, USA.
          [2 ] Department of Internal Medicine, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
          [3 ] Department of Biomedical Sciences, New York Institute of Technology - College of Osteopathic Medicine, Old Westbury, New York, New York, USA.
          Article
          000471938
          10.1159/000471938
          28376489
          833141df-d34a-4451-abb6-74968dc37b8a
          © 2017 The Author(s)Published by S. Karger AG, Basel.
          History

          Endothelial cell,Non-genomic effect,PKG,Triiodothyronine (T3),Vascular smooth muscle cell,Vasorelaxation,p-VASP

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