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Role of CaMKII in Ang-II-dependent small artery remodeling
Journal article   Open access   Peer reviewed

Role of CaMKII in Ang-II-dependent small artery remodeling

Anand M Prasad, Pimonrat Ketsawatsomkron, Daniel W Nuno, Olha M Koval, Megan E Dibbern, Ashlee N Venema, Curt D Sigmund, Kathryn G Lamping and Isabella M Grumbach
Vascular pharmacology, Vol.87, pp.172-179
12/2016
DOI: 10.1016/j.vph.2016.09.007
PMCID: PMC5164857
PMID: 27658984
url
https://doi.org/10.1016/j.vph.2016.09.007View
Published (Version of record) Open Access

Abstract

Angiotensin-II (Ang-II) is a well-established mediator of vascular remodeling. The multifunctional calcium-calmodulin-dependent kinase II (CaMKII) is activated by Ang-II and regulates Erk1/2 and Akt-dependent signaling in cultured smooth muscle cells in vitro. Its role in Ang-II-dependent vascular remodeling in vivo is far less defined. Using a model of transgenic CaMKII inhibition selectively in smooth muscle cells, we found that CaMKII inhibition exaggerated remodeling after chronic Ang-II treatment and agonist-dependent vasoconstriction in second-order mesenteric arteries. These findings were associated with increased mRNA and protein expression of smooth muscle structural proteins. As a potential mechanism, CaMKII reduced serum response factor-dependent transcriptional activity. In summary, our findings identify CaMKII as an important regulator of smooth muscle function in Ang-II hypertension in vivo. [Display omitted]
Smooth muscle CaMKII Ang-II Remodeling

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