The anti‐atherosclerotic di‐peptide, Trp‐His, inhibits the phosphorylation of voltage‐dependent L‐type Ca<sup>2+</sup>channels in rat vascular smooth muscle cells
書誌事項
- 公開日
- 2012-01
- 資源種別
- journal article
- 権利情報
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- http://creativecommons.org/licenses/by-nc-nd/3.0/
- http://doi.wiley.com/10.1002/tdm_license_1
- http://doi.wiley.com/10.1002/tdm_license_1.1
- DOI
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- 10.1016/j.fob.2012.04.005
- 公開者
- Wiley
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説明
<jats:p>Trp‐His is the only vasoactive di‐peptide known to regulate intracellular Ca<jats:sup>2+</jats:sup>([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) and prevent the onset of atherosclerosis in mice. In this study, we showed that Trp‐His reduced the [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>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<jats:sup>2+</jats:sup>channels (VDCC). Therefore, Trp‐His potentially regulates the VDCC phosphorylation cascade through Ca<jats:sup>2+</jats:sup>‐CaM/CaMK II.</jats:p>
収録刊行物
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- FEBS Open Bio
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FEBS Open Bio 2 (1), 83-88, 2012-01
Wiley
