Ischemia-reperfusion or traumatic brain injury induces the accumulation of reactive oxygen species (ROS) in brain. ROS causes oxidative stress to astrocytes as well as neurons and oxidative stress induces the damage to organelles, proteins or lipids. The removal of damaged cellular cytosolic components is indispensable for the cell to keep the homeostasis. Macroautophagy (hereafter referred to as autophagy) is the process to degrade defective proteins and damaged organelles. In the process of autophagy, damaged cellular cytosolic components are isolated by autophagosomes. Microtubule-associated protein 1 light chain 3B (LC3B) plays a significant role in the autophagosome formation, and the conversion from unconjugated-LC3B (LC3B-I) to phosphatidylethanolamine (PE) conjugated-LC3B (LC3B-II) is the index of the activitation of autophagy. GABARAPL1 is the paralogue of LC3B and the function of GABARAPL1 is not fully understood.

In this study, we demonstrated GABARAPL1 mRNA and protein expression are up-regulated by H₂O₂ in rat C6 glioma cells and the induction of GABARAPL1 by H₂O₂ was accompanied with the conversion from LC3B-I to LC3B-II, indicating the formation of autophagosomes. Thus, GABARAPL1 may play a role in autophagic process, which is induced by H₂O₂. However, elucidation of the function of GABARAPL1 in autophagy will require further studies.