ArticleFEBS open bio2012
The anti-atherosclerotic di-peptide, Trp-His, inhibits the phosphorylation of voltage-dependent L-type Ca(2+) channels in rat vascular smooth muscle cells.
Article in FEBS open bio, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Indole metabolism and its role in diabetic macrovascular and microvascular complications.American heart journal plus : cardiology research and practice · 2025Review
- Adenine attenuates the Ca(2+) contraction-signaling pathway via adenine receptor-mediated signaling in rat vascular smooth muscle cells.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- GABAB receptors are expressed in human aortic smooth muscle cells and regulate the intracellular Ca(2+) concentration.Heart and vessels · 2015Article
- Vasorelaxing and antihypertensive activities of synthesized peptides derived from computer-aided simulation of pepsin hydrolysis of yam dioscorin.Botanical studies · 2014Article
- Article
- The di-peptide Trp-His activates AMP-activated protein kinase and enhances glucose uptake independently of insulin in L6 myotubes.FEBS open bio · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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