Introdunction The serine/threonine kinase, LKB1 tumor suppressor are associated with Peutz-Jegher's syndrome. LKB1 is involved in the regulation of cellular proliferation, apoptosis and cellular energy metabolism. The mice with a targeted disruption of LKB1 die at midgestation showing severe vascular abnormalities. We observed the expression of LKB1 in the vascular smooth muscle cells (VSMCs) and neointima of injured rat carotid artery is associated with VSMC proliferation and neointima formation. Results Angiotensin II (Ang II) is one of the stimulator of VSMCs proliferation. LKB1 expression was increased by Ang II in the cultured rat VSMCs in a time- and dose-dependent manner. We harvested carotid artery several days after rat carotid balloon injury and perfused for immunohistochemistry, homogenized for western blot. The post-injury neointima formation was significantly increased in balloon injury group compared with sham operation. The expression of LKB1 was more decreased than sham operation (p<0.05). The activity of LKB1 was significantly decreased 2 days after carotid balloon injury(p<0.05). The decreased activy of LKB1 was continued 14 days after balloon injury. Conclusion The LKB1 activity was decreased after carotid artery injury and increased by Ang II. The LKB1 might be one of the regulator of VSMC proliferation and neointima formation.