Interferon‐β enhances autophagy of vascular smooth muscle cells

Autophagy, type 2 programmed cell death, is a self‐digestion process that degrades intracellular structures in response to stresses leading to cell survival. Autophagy also is a special pathway leading to cell death in atherosclerotic vessels, and cells die with a morphology that is intermediate between apoptosis and necrosis. Previous studies have documented that cytokines induces autophagy. However, the role of Interferon‐β (IFN‐β) in autophagy is unknown. In the present study, we reported that IFN‐β with potent antiviral and anti‐proliferative activities up‐regulated autophagy in vascular smooth muscle cells (VSMCs). After 3 days of IFN‐β treatment under serum free condition, flow cytometry analysis showed that IFN‐β at 2000U/ml increased the ROS production. In addition, western blot analysis revealed that treatment with IFN‐β resulted in increase in the expression of LC3‐¥± which is a widely used marker of autophagy. The present data also demonstrated that IFN‐β increased in the expression of autophagy‐related gene 5 (Atg5) and Atg6/Beclin‐1. Moreover, the levels of Rab5 and Rab7 protein that are regulators of autophagosome formation were up‐regulated by IFN‐β. Thus, these results suggest that IFN‐β regulates autophagy‐related genes expression and ROS production, leading to induction of autophagy in VSMCs.