Effects of c-Jun N-terminal kinase on Activin A/Smads signaling in PC12 cell suffered from oxygen-glucose deprivation
Corresponding Author(s) : J Q Wang
Cellular and Molecular Biology,
Vol. 62 No. 2: Issue 2
Activin A (Act A), a member of transforming growth factor-Î² (TGF-Î²) 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-Î² 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.
JNK Activin A Smads Oxygen–Glucose Deprivation (OGD).
Wang, J. Q., Xu, Z. H., Liang, W. Z., He, J. T., Cui, Y., Liu, H. Y., Xue, L. X., Shi, W., Shao, Y. K., Mang, J., & Xu, Z. X. (2016). Effects of c-Jun N-terminal kinase on Activin A/Smads signaling in PC12 cell suffered from oxygen-glucose deprivation. Cellular and Molecular Biology, 62(2), 81–86. Retrieved from https://cellmolbiol.org/index.php/CMB/article/view/804
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