Astrocytes play an important role in the central nervous system. Ischemia, hypoxia, and traumatic injury cause mitochondrial damage in neurons and astrocytes. Damaged mitochondria are isolated and removed by macroautophagy (hereafter referred to as autophagy), which degrades cellular components with autophagosomes. Autophagy that removes mitochondria is called mitophagy. Phosphatidylethanolamine (PE)-conjugated microtubule-associated protein 1 light chain 3B (LC3B) (LC3B-II) plays a crucial

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... in the formation of autophagosomes, and the conversion of unconjugated-LC3B (LC3B-I) to LC3B-II is the index of the induction of autophagy. Gamma-aminobutyric acid receptor-associated protein-like 2 (GABARAPL2) is the paralog of LC3B, and its function is not clear. In this study, we demonstrated that both the expression of total GABARAPL2 and the conversion of unconjugated-GABARAPL2 (GABARAPL2-I) to PE-conjugated GABARAPL2 (GABARAPL2-II) were upregulated by carbonyl cyanide 3-chlorophenylhydrazine (CCCP), which induces mitochondrial dysfunction and fragmentation. In contrast, CCCP upregulated the conversion of LC3B-I to LC3B-II, but it did not affect the expression of total LC3B. Thus, GABARAPL2 might function in the process of mitophagy during the formation of autophagosomes, and the expressions of GABARAPL2 and LC3B were regulated differently. The mechanism underlying the role of GABARAPL2 in mitophagy requires further investigations.