Activin A/Smads signaling pathway negatively regulates Oxygen Glucose Deprivation-induced autophagy via suppression of JNK and p38 MAPK pathways in neuronal PC12 cells
- Biochem Biophys Res Commun. 2016 Nov 18;480(3):355-361. doi: 10.1016/j.bbrc.2016.10.050.
- 1. Department of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun 130012, China.
- 2. Clinical Medicine of Norman Bethune Medical Department, Jilin University, Changchun 130012, Jilin Province, China.
- 3. Research Center, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun 130012, China.
- 4. Department of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun 130012, China. Electronic address: [email protected].
- 5. Department of Neurology, China-Japan Union Hospital, Jilin University, 126 Xiantai Street, Changchun 130012, China. Electronic address: [email protected].
Activin A (Act A), a member of the transforming growth factor-beta (TGF-β), reduces neuronal Apoptosis during cerebral ischemia through Act A/Smads signaling pathway. However, little is known about the effect of Act A/Smads pathway on Autophagy in neurons. Here, we found that oxygen-glucose deprivation (OGD)-induced Autophagy was suppressed by exogenous Act A in a concentration-dependent manner and enhanced by Act A/Smads pathway inhibitor (ActRIIA-Ab) in neuronal PC12 cells. These results indicate that Act A/Smads pathway negatively regulates Autophagy in OGD-treated PC12 cells. In addition, we found that c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein (MAP) kinase pathways are involved in the OGD-induced Autophagy. The activation of JNK and p38 MAPK pathways in OGD-treated PC12 cells was suppressed by exogenous Act A and enhanced by ActRIIA-Ab. Together, our results suggest that Act A/Smads signaling pathway negatively regulates OGD-induced Autophagy via suppression of JNK and p38 MAPK pathways in neuronal PC12 cells.