Expression of Cyclin-Dependent Kinase Inhibitors in Vascular Disease

摘要: Arterial lesions in cardiovascular diseases are characterized by proliferation and migration of smooth muscle cells as well deposition connective tissue matrix. Factors that stimulate vascular cell (VSMC) described; however, the role proteins limit intimal hyperplasia is not understood. To examine function Kip/Cip INK cyclin-dependent kinase inhibitors (CKIs) diseases, expression p27Kip1 p16INK was examined VSMCs vitro porcine arteries human atherosclerosis vivo. Western blot fluorescence activated cell-sorting analysis demonstrated levels p27Kip1, but p16INK, increased during serum deprivation primary VSMC cultures caused G1 arrest. inhibited Cdk2 activity, suggesting Kip CKIs promote arrest binding cyclin E/Cdk2. In arteries, constitutively expressed at low levels. Immediately after balloon injury, declined. Three weeks strongly when < 2%, functions an inhibitor injured arteries. contrast, detected only transiently early injury. CKI 35 coronary ranging from normal to advanced atherosclerosis. abundant nonproliferating macrophages within (7 8) atherosclerotic (25 27) p21Cip1 were undetectable elevated (19 could be or (0 35). Thus, have different temporal patterns contrast likely contributes remodeling process phase cycle.