title: The anti-atherosclerotic di-peptide, Trp-His, inhibits the phosphorylation of voltage-dependent L-type Ca(2+) channels in rat vascular smooth muscle cells.
abstract: 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.
authors: Department of Bioscience and Biotechnology, Faculty of Agriculture, Graduate School of Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan.
authors: Yutaro
authors: Y
authors: Kobayashi
authors: Toshihiko
authors: T
authors: Fukuda
authors: Mitsuru
authors: M
authors: Tanaka
authors: Toshiro
authors: T
authors: Matsui
keywords: 2-APB, 2-aminoethoxydiphenyl borate; AT2R, angiotensin type 2 receptor; Ang II, angiotensin II; CaMK II, calmodulin-dependent kinase II; Calmodulin-dependent kinase II; Di-peptide; ER/SR, endoplasmic reticulum/sarcoplasmic reticulum; IP3R, inositol 1,4,5-trisphosphate receptor; Intracellular Ca2+; L-type Ca2+ channel; PLC, phospholipase C; Phos-tag; VDCC, voltage-dependent L-type Ca2+ channels; VSMCs, vascular smooth muscle cells
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