Cellular subtype expression and activation of CaMKII regulate the fate of atherosclerotic plaque.

Authors:
Angela Serena Maione
Angela Serena Maione
University of Naples Federico II
Italy
Ersilia Cipolletta
Ersilia Cipolletta
Department of Clinical Medicine
Italy
Daniela Sorriento
Daniela Sorriento
Department of Clinical Medicine
Italy
Francesco Borriello
Francesco Borriello
Department of Clinical and Experimental Medicine
Italy
Maria Soprano
Maria Soprano
Federico II University
Napoli | Italy
Maria Rosaria Rusciano
Maria Rosaria Rusciano
University of Naples Federico II
Italy
Abdul Karim Markabaoui
Abdul Karim Markabaoui
Federico II University
Napoli | Italy

Atherosclerosis 2017 01 5;256:53-61. Epub 2016 Nov 5.

Department of Translational Medical Science, Federico II University, Naples, Italy; Federico II University and Hospital, Naples, Italy. Electronic address:

Background And Aims: Atherosclerosis is a degenerative process of the arterial wall implicating activation of macrophages and proliferation of vascular smooth muscle cells. Calcium-calmodulin dependent kinase type II (CaMKII) in vascular smooth muscle cells (VSMCs) regulates proliferation, while in macrophages, this kinase governs diapedesis, infiltration and release of extracellular matrix enzymes. We aimed at understanding the possible role of CaMKII in atherosclerosis plaques to regulate plaque evolution towards stability or instability.

Methods: Clinically defined stable and unstable plaques obtained from patients undergoing carotid end arteriectomy were processed for evaluation of CaMKs protein expression, activity and localization.

Results: The larger content of CaMKII was found in CD14myeloid cells that were more abundant in unstable rather than stable plaques. To test the biological effect of activated CD14myeloid cells, VSMCs were exposed to the conditioned medium (CM) of macrophages extracted from carotid plaques. CM induced attenuation of CaMKs expression and activity in VSMCs, leading to the reduction of VSMCs proliferation. This appears to be due to the CaMKII dependent release of cytokines.

Conclusions: These results indicate a pivotal role of CaMKs in atherosclerosis by regulating activated myeloid cells on VSMCs activity. CaMKII could represent a possible target for therapeutic strategies based on macrophages specific inhibition for the stabilization of arteriosclerotic lesions.

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http://dx.doi.org/10.1016/j.atherosclerosis.2016.11.006DOI Listing

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January 2017
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