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Cardiovascular Research Advance Access [Accepted Manuscript] published online on September 18, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm010
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CaM Kinase II-Dependent Pathophysiological Signaling in Endothelial Cells

Hua Cai*,, Depei Liu& and Joe G.N. Garcia#

* Division of Molecular Medicine, Cardiovascular Research Laboratories, Departments of Anesthesiology and Medicine, David Geffen School of Medicine, University of California Los Angeles (UCLA), Los Angeles, CA
& National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College
# Section of Pulmonary and Critical Care Medicine, Department of Medicine, The Division of Biological Sciences and Pritzker School of Medicine, The University of Chicago, Chicago, IL

Address Correspondence to: Hua Linda Cai, MD, PhD, Division of Molecular Medicine, Cardiovascular Research Laboratories, Departments of Anesthesiology and Medicine, David Geffen School of Medicine, University of California Los Angeles (UCLA), 650 Charles E Young Drive, BH550 CHS, Los Angeles, CA, 90095, Tel: 310-267-2303, Fax: 310-825-0132, Email: hcai{at}mednet.ucla.edu

Calcium/calmodulin-dependent protein kinase II (CaM Kinase II) is a known modulator of cardiac pathophysiology. The present review uniquely focuses on novel CaM Kinase II-mediated endothelial cell signaling which, under pathophysiological conditions, may indirectly modulate cardiac functions via alterations in endothelial or endocardial responses. CaM Kinase II has four different isoforms and various splicing variants for each isoform. The endothelial cell CaM Kinase II isoforms are sensitive to KN93 and a threonine 286-mutated inhibitory peptide. In macro- vascular endothelial cells derived from aortas, CaM Kinase II mediates redox-sensitive upregulation of endothelial nitric oxide synthase (eNOS) gene expression by hydrogen peroxide (H2O2) and oscillatory shear stress, and a rapid activation of eNOS in response to bradykinin. In endothelial cells derived from lung microvessels, CaM Kinase II mediates barrier dysfunction, particularly when activated by thrombin. In brain capillary endothelial cells, CaM Kinase II lies upstream of voltage-gated potassium channels and hypoxia induced cell swelling. In both macrovascular and microvascular endothelial cells, CaM Kinase II mediates actin cytoskeleton reorganization via distinct p38MAPK/HSP27 and ERK1/2/MLCK signaling pathways, respectively. Although understanding of endothelium-specific CaM Kinase II signaling is nascent, data accumulated so far have demonstrated a potentially significant role of CaM Kinase II in endothelial cell pathophysiology.

KEYWORDS CaM Kinase II; endothelial nitric oxide synthase (eNOS); hydrogen peroxide; shear stress; actin cytoskeleton; barrier function; thrombin; bradykinin

Time for primary review: 26 days


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