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

摘要: Abstract Background and aims Atherosclerosis is a degenerative process of the arterial wall implicating activation macrophages proliferation vascular smooth muscle cells. Calcium-calmodulin dependent kinase type II (CaMKII) in cells (VSMCs) regulates proliferation, while macrophages, this governs diapedesis, infiltration release extracellular matrix enzymes. We aimed at understanding possible role CaMKII atherosclerosis plaques to regulate plaque evolution towards stability or instability. Methods Clinically defined stable unstable obtained from patients undergoing carotid end arteriectomy were processed for evaluation CaMKs protein expression, activity localization. Results The larger content was found CD14 + myeloid that more abundant rather than plaques. To test biological effect activated cells, VSMCs exposed conditioned medium (CM) extracted CM induced attenuation expression VSMCs, leading reduction proliferation. This appears be due cytokines. Conclusions These results indicate pivotal by regulating on activity. could represent target therapeutic strategies based specific inhibition stabilization arteriosclerotic lesions.