Angiotensin II has been implicated in vascular remodeling. Microtubule composed 
of tubulins regulates cell shape, migration and survival. Tubulin acetylation 
has an important role in the control of microtubule structure and 
microtubule-based cellular functions. In this study, angiotensin II induced 
disassembly and deacetylation of α-tubulin, which were blocked by pretreatment 
with an angiotensin II type 1 receptor blocker losartan and a sirtuin class 
deacetylase inhibitor sirtinol, and by depletion of a deacetylase SIRT2 using 
RNA interference. We investigated the involvement of SIRT2 in angiotensin 
II-induced endothelial cell migration using the Boyden chamber method. 
Angiotensin II caused a significant increase in cell migration, which was 
blocked by pretreatment with sirtinol and SIRT2 depletion. It has been reported 
that angiotensin II is involved in cytoskeletal reorganization stimulated by 
mechanical stretch in endothelial cells. We also demonstrated that endothelial 
cells subjected to a 10% uniaxial stretch showed vertical alignment to the 
direction of tension and tubulin deacetylation in the peripheral side of cells, 
in comparison with control static cells. The mechanical stretch-induced changes 
of microtubules were blocked by pretreatment with sirtinol and SIRT2 depletion. 
Immunofluorescence microscopy showed that acetylated tubulin was decreased in 
platelet-endothelial cell adhesion molecule-1-positive cells in the intima of 
the aortic walls in mice loaded with angiotensin II, in comparison with mice 
loaded with control vehicle. These data show that angiotensin II and mechanical 
stretch stimulate microtubule redistribution and deacetylation via SIRT2 in 
endothelial cells, suggesting the emerging role of SIRT2 in hypertension-induced 
vascular remodeling.