Open AccessThe anti‐atherosclerotic di‐peptide, Trp‐His, inhibits the phosphorylation of voltage‐dependent L‐type Ca 2+ channels in rat vascular smooth muscle cells
Author(s) -
Kobayashi Yutaro,
Fukuda Toshihiko,
Tanaka Mitsuru,
Matsui Toshiro
Publication year - 2012
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1016/j.fob.2012.04.005
Subject(s) - vascular smooth muscle , phosphorylation , angiotensin ii , chemistry , peptide , calmodulin , phospholipase c , protein kinase a , intracellular , voltage dependent calcium channel , protein kinase c , microbiology and biotechnology , medicine , biochemistry , endocrinology , calcium , biology , signal transduction , smooth muscle , receptor , enzyme , organic chemistry
Trp‐His is the only vasoactive di‐peptide known to regulate intracellular Ca 2+ ([Ca 2+ ] i ) and prevent the onset of atherosclerosis in mice. In this study, we showed that Trp‐His reduced the [Ca 2+ ] i elevation in phospholipase C‐activated vascular smooth muscle cells (VSMCs), while a mixture of the corresponding constituent amino acids did not show significant reduction. Furthermore, Trp‐His suppressed calmodulin‐dependent kinase II (CaMK II) activity in angiotensin II‐stimulated VSMCs, resulting in the inhibition of phosphorylation of voltage‐dependent L‐type Ca 2+ channels (VDCC). Therefore, Trp‐His potentially regulates the VDCC phosphorylation cascade through Ca 2+ ‐CaM/CaMK II.