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Modulation of arginases by different patterns of shear stress: new signaling pathway in atherogenesis?

Atherosclerosis is influenced by a variety of environmental, humoral, and genetic factors. While these risk factors act systemically on the entire vascular system, it is increasingly recognized that hemodynamic factors act at particular locations of the vessels, favouring the focal development of vascular lesions. Alterations of wall shear stress, the frictional force generated by blood flow, can predispose the endothelium to the development of atherosclerotic plaques and determine its lesion size and phenotype. A body of evidence indicates that arginase expression and/or activity correlates with several risk factors for cardiovascular disease in humans. And it has been recently reported that higher arginase enzyme activity is involved in endothelial dysfunction in apolipoprotein E-deficient (ApoE–/–) mice (Ming et al. 2004). So far, the regulation of the arginase pathway by shear stress patterns has not yet been investigated. In the present work we hypothesize that arginases are differentially modulated by particular patterns of shear stress, which in turn may play an important role in the process of shear stress-induced plaque formation and vulnerability.