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Biochem Biophys Res Commun. 2011 Feb 4;405(1):47-51. doi: 10.1016/j.bbrc.2010.12.120. Epub 2010 Dec 30.

Exploring calmodulin-related proteins, which mediate development of hypertension, in vascular tissues of spontaneous hypertensive rats.

Author information

1
Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Towada, Aomori, Japan.

Abstract

Calmodulin (CaM) is associated with a variety of cell functions including inflammation, apoptosis, and muscular contraction. It is recently clarified that some CaM-related proteins are responsible for cardiovascular diseases. We therefore explored CaM-related proteins that mediate hypertensive vascular diseases. Expression levels of six CaM-related proteins with almost unknown function in blood vessels were examined in aorta and mesenteric artery from spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) by Western blotting. In aorta from SHR, eukaryotic elongation factor (eEF)2 kinase (eEF2K) and death-associated protein kinase (DAPK)3 protein increased compared with WKY, while Ca(2+)/CaM-dependent protein kinase IIδ, histone deacetylases (HDAC)4 and HDAC5 protein decreased. In mesenteric artery from SHR, eEF2K, HDAC4 and DAPK3 protein increased compared with WKY, while HDAC5 decreased. Our findings demonstrate that expression levels of several CaM-related proteins are changed in vascular tissues of SHR and suggest that CaM-related proteins might be at least in part related to the pathogenesis of hypertensive vascular diseases.

PMID:
21195054
DOI:
10.1016/j.bbrc.2010.12.120
[Indexed for MEDLINE]

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