@article{Wang_Xu_Liang_He_Cui_Liu_Xue_Shi_Shao_Mang_Xu_2016, title={Effects of c-Jun N-terminal kinase on Activin A/Smads signaling in PC12 cell suffered from oxygen-glucose deprivation}, volume={62}, url={https://cellmolbiol.org/index.php/CMB/article/view/804}, abstractNote={Activin A (Act A), a member of transforming growth factor-β (TGF-β) superfamily, is an early gene in response to cerebral ischemia. Growing evidences confirm the neuroprotective effect of Act A in ischemic injury through Act A/Smads signal activation. In this process, regulation networks are involved in modulating the outcomes of Smads signaling. Among these regulators, crosstalk between c-Jun N-terminal kinase (JNK) and Smads signaling has been found in the TGF-β induced epithelial-mesenchymal transition. However, in neural ischemia, the speculative regulation between JNK and Act A/Smads signaling pathways has not been clarified. To explore this issue, an Oxygen Glucose Deprivation (OGD) model was introduced to nerve-like PC12 cells. We found that JNK signal activation occurred at the early time of OGD injury (1 h). Act A administration suppressed JNK phosphorylation. In addition, JNK inhibition could elevate the strength of Smads signaling and attenuate neural apoptosis after OGD injury. Our results indicated a negative regulation effect of JNK on Smads signaling in ischemic injury. Taken together, JNK, as a critical site for neural apoptosis and negative regulator for Act A/Smads signaling, was presumed to be a molecular therapeutic target for ischemia.}, number={2}, journal={Cellular and Molecular Biology}, author={Wang, J Q and Xu, Z H and Liang, W Z and He, J T and Cui, Y and Liu, H Y and Xue, L X and Shi, W and Shao, Y K and Mang, J and Xu, Z X}, year={2016}, month={Feb.}, pages={81–86} }