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Published on: September 22, 2011
Exploring calmodulin-related proteins, which mediate development of hypertension, in vascular tissues of spontaneous
Tatsuya Usui1, Muneyoshi Okada, Yukio Hara
1Laboratory 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.
Insights
Calmodulin-related proteins are altered in hypertensive rats, suggesting their role in the development of hypertensive vascular diseases. This study investigated changes in specific proteins within blood vessels of spontaneously hypertensive rats.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Biochemistry
Background:
- Calmodulin (CaM) regulates critical cellular functions, including inflammation, apoptosis, and muscle contraction.
- Emerging evidence links CaM-related proteins to cardiovascular diseases.
- The specific role of CaM-related proteins in hypertensive vascular diseases remains largely unexplored.
Purpose of the Study:
- To investigate the expression levels of six CaM-related proteins in the vascular tissues of spontaneously hypertensive rats (SHR).
- To determine if altered expression of these proteins contributes to the pathogenesis of hypertensive vascular diseases.
Main Methods:
- Western blotting was employed to quantify protein expression.
- Aorta and mesenteric artery tissues were analyzed from SHR and normotensive Wistar Kyoto rats (WKY).
Main Results:
- In the aorta of SHR, increased expression of eukaryotic elongation factor 2 kinase (eEF2K) and death-associated protein kinase (DAPK)3 was observed compared to WKY.
- Conversely, Ca(2+)/CaM-dependent protein kinase IIδ, histone deacetylase (HDAC)4, and HDAC5 protein levels decreased in the aorta of SHR.
- In mesenteric arteries, eEF2K, HDAC4, and DAPK3 showed increased expression, while HDAC5 decreased in SHR compared to WKY.
Conclusions:
- Expression levels of several CaM-related proteins are significantly altered in the vascular tissues of SHR.
- These findings suggest that CaM-related proteins play a role in the development of hypertensive vascular diseases.
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