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

Sherin Samuel | Zendy; Kuo Zhang | Zendy; YiDa Tang | Zendy; A. Martin Gerdes | Zendy; Maria Alícia Carrillo-Sepúlveda | Zendy

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

Author(s) -

Sherin Samuel,

Kuo Zhang,

YiDa Tang,

A. Martin Gerdes,

Maria Alícia Carrillo-Sepúlveda

Publication year - 2017

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000471938

Subject(s) - vascular smooth muscle , myograph , cgmp dependent protein kinase , sodium nitroprusside , nitric oxide , chemistry , phosphorylation , medicine , microbiology and biotechnology , endocrinology , signal transduction , enos , soluble guanylyl cyclase , protein kinase a , nitric oxide synthase , biology , smooth muscle , cyclin dependent kinase 2 , guanylate cyclase

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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