NDLI: Differential effects of p38 and JNK activation by GSK3 on cadmium-induced autophagy and apoptosis

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Toxicology Research Vol - 4 Issue - 3

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Differential effects of p38 and JNK activation by GSK3 on cadmium-induced autophagy and apoptosis

Content Provider	Royal Society of Chemistry (RSC)
Author	Kim, Seong-Hwan An, Tae-Hun Lee, Hyun-Young Oh, Seon-Hee Kim, Hak-Ryul Jung, Ki-Tae So, Keum-Young Lee, Byung-Hoon
Copyright Year	2015
Abstract	Cadmium (Cd) toxicity is associated with endoplasmic reticulum (ER) stress-mediated apoptosis and autophagy. However, the regulatory mechanisms responsible for the signaling pathways initiated by Cd are incompletely understood. Here, we investigated the involvement of glycogen synthase kinase (GSK) 3αβ and mitogen-activated protein kinases (MAPKs) in Cd toxicity. Cd-exposed H460 cells exhibited activation of JNK, p38, PERK, and CHOP and induction of autophagy and apoptosis; in contrast, levels of these proteins were minimal in Cd-resistant H1299 cells. In H460 cells, genetic or pharmacological inhibition of JNK markedly enhanced CHOP, autophagy and apoptosis induced by Cd, which were reversed by overexpression of JNK1. Inhibition of p38 suppressed Cd-induced CHOP, and markedly inhibited autophagy via Atg5 downregulation. Cd-exposed H460 cells showed GSK3αβ phosphorylation at serine (Ser) and tyrosine (Tyr) residues, which was downregulated by a GSK3 inhibitor (SB216763) and by genetic silencing of GSK3β, subsequently suppressing JNK and p38 activation. However, H460 cells pretreated with lithium or overexpressing GSK3β exhibited enhanced JNK and p38 activation. Pretreatment of H460 cells with okadaic acid (a Ser/Thr phosphatase inhibitor) upregulated Cd-induced p-Ser GSK3αβ and enhanced CHOP, p-p38 and autophagy, whereas treatment with vanadate (a tyrosine phosphatase inhibitor) downregulated Cd-induced p-Ser GSK3αβ, enhanced p-JNK and downregulated CHOP and autophagy. Furthermore, H460 cells overexpressing a constitutively active GSK3β mutant (S9A) exhibited enhanced p-JNK and inhibited CHOP, whereas overexpression of constitutively inactive GSK3β (K85A) enhanced p-p38 and autophagy in response to Cd. Pretreatment with N-acetyl cysteine suppressed Cd-induced p-Ser/p-Tyr GSK3αβ and downstream pathways. These findings show that Cd toxicity is regulated by autophagy, which can be countered by prosurvival JNK and prodeath p38 MAPK activation through site-specific phosphorylation of GSK3αβ.
Starting Page	976
Ending Page	985
Page Count	10
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	4
Issue Number	4
Journal	Toxicology Research
DOI	10.1039/c5tx00007f
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Tyrosine Cadmium GSK3B Phosphorylation Protein tyrosine phosphatase Serine Enzyme inhibitor Acetylcysteine Mitogen-activated protein kinase Lithium GSK-3 Phosphatase Autophagy Protein Vanadate MAPK8 Carboxylic acid P38 mitogen-activated protein kinases C-Jun N-terminal kinases CHOP Mutation Endoplasmic reticulum Apoptosis
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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Correction: Differential effects of p38 and JNK activation by GSK3 on cadmium-induced autophagy and apoptosis

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Differential effects of p38 and JNK activation by GSK3 on cadmium-induced autophagy and apoptosis

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