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Neurotoxicology

Neurotoxicology

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Positive regulation of the CREB phosphorylation via JNK-dependent pathway prevents antimony-induced neuronal apoptosis in PC12 cell and mice brain.

Published:1 December 2020 DOI: PMID: 32920012
Ye Zhi , Chunhua Lu , Ganlin Zhu , Zhijie Li , Piaoyu Zhu , Yuting Liu , Weiwei Shi , Liling Su , Junkang Jiang , Jianhua Qu , Xinyuan Zhao

Abstract

Antimony (Sb) is a potentially toxic chemical element abundantly found in the environment. We previously reported that Sb promoted neuronal deathvia reactive oxygen species-dependent autophagy. Here, we assessed the role of cyclic adenosine monophosphate response element-binding protein (CREB) in Sb-induced neuronal damage. We found that Sb treatment induced CREB phosphorylation and neuronal apoptosis both in vitro and in vivo. Interestingly, inhibition of CREB’s transcriptional activity with 666?15 dramatically enhanced apoptosis in PC12 cells by downregulating B-cell lymphoma 2 (Bcl-2). Additionally, Sb activated ERK, JNK, and p38 signaling ; however, only JNK promoted CREB phosphorylation. In conclusion, our findings suggest that CREB phosphorylation by JNK attenuates Sb-induced neuronal apoptosis via Bcl-2 upregulation. These data suggest that JNK-dependent CREB activation prevents neurons from Sb-induced apoptosis and guides the development of novel strategies to prevent Sb-induced neurotoxicity.

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Materials Related products
Procduct Name CAS Molecular Formula Supplier Price
CREB inhibitor (666-15) 1433286-70-4 C33H31Cl2N3O5 72 suppliers $62.00-$2400.00
CREB inhibitor (666-15) 1433286-70-4 C33H31Cl2N3O5 72 suppliers $62.00-$2400.00
CREB inhibitor (666-15) 1433286-70-4 C33H31Cl2N3O5 72 suppliers $62.00-$2400.00
CREB inhibitor (666-15) 1433286-70-4 C33H31Cl2N3O5 72 suppliers $62.00-$2400.00

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