Research articleThrombin preferentially induces autophagy in glia cells in the rat central nervous system

•Thrombin activates beclin1 expression preferentially in astrocytes.•Thrombin induces astrocytic, but not neuronal, vacuole formation.•Thrombin increases the level of LC3II and MDC+ cells in cultured astrocytes.

Autophagy widely occurs after intracerebral hemorrhage (ICH). In our previous study, we demonstrated that thrombin, a serine protease produced after hematoma, contributes to ICH-induced autophagy. However, whether thrombin plays a neuronal and/or astrocytic role in autophagy induction is largely unknown. Here, we examined the autophagic role of thrombin on neurons and glia cells, respectively. In vivo, we found that intracaudate injection of thrombin specifically elevated the astrocytic expression of beclin-1 and LC3, two autophagic markers, and promoted the formation of autophagic vacuoles within astrocytes rather than neurons in the ipsilateral basal ganglia. Consistent with this, thrombin enhanced the LC3-II level and increased the number of MDC-labeled autophagic vacuoles in cultured astrocytes. These results indicated that thrombin preferentially activated astrocytic autophagy after ICH, and therefore provided novel insights into the pathophysiological mechanisms and therapeutic targets for hemorrhage stroke and brain trauma.