622-P: Mechanism of Lin28a Promoting Vascular Smooth Muscle Cell Proliferation and Migration in Restenosis

Background: Restenosis (RS) after percutaneous transluminal angioplasty severely affects the curative effect of patients with lower extremity peripheral arterial disease. Our previous research indicated that abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) was the key factor in the RS plaque formation. The process of Lin28a regulating cell proliferation demonstrates similarities with the proliferation of VSMCs in RS. Here, we aim to explore the specific role of Lin28a in RS. Methods: To distinguish from atherosclerotic lesions, RS and atherosclerosis (AS) models were simultaneously established in type 2 diabetic rats. Lin28a level in VSMCs was detected by immunofluorescence double staining. The changes of VSMCs were determined when modulating Lin28a in vivo and vitro and downstream mechanism was further explored. Results: Thirty-two folds higher level of Lin28a was found in VSMCs in RS compared with AS (P