Faculty Collaboration Database

Role of CaMKII in Ang-II-dependent small artery remodeling. Vascul Pharmacol 2016 Dec;87:172-179

Date

09/24/2016

Pubmed ID

27658984

Pubmed Central ID

PMC5164857

DOI

10.1016/j.vph.2016.09.007

Scopus ID

2-s2.0-84999885129 (requires institutional sign-in at Scopus site)   5 Citations

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.

Author List

Prasad AM, Ketsawatsomkron P, Nuno DW, Koval OM, Dibbern ME, Venema AN, Sigmund CD, Lamping KG, Grumbach IM

Author

Curt Sigmund PhD Chair, Professor in the Physiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Angiotensin II
Animals
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Female
Male
Mesenteric Arteries
Mice
Mice, Inbred C57BL
Mice, Transgenic
Muscle, Smooth, Vascular
Myocytes, Smooth Muscle
RNA, Messenger
Vascular Remodeling
Vasoconstriction