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Overexpression of p58ipk protects neuroblastoma against paraquat-induced toxicity
Fengrui Li1,2, Biao Ge3, Alatangaole Damirin1
1School of Life Sciences, Inner Mongolia University Hohhot 010021, China.
Background:
Paraquat (PQ) is a powerful pathologic pesticide that contribute to the neurotoxicity, however, the pathogenic mechanism between them was unclear. The aims of this study were to explore the underlying mechanism of PQ-induced toxicity and then make potential contribute to such neuronal diseases therapy.
Methods:
Human cell line SH-SY5Y was pretreated with a set concentrations of PQ to detect the cell apoptosis and the expression of related genes and proteins. Next, pcDNA 3.1-p58ipk or si-p58ipk was transfected the PQ-induced cells to detect the cytotoxicity.
Results:
PQ significantly increased the cell apoptosis as well as the expression of p58ipk and CHOP, but decreased the expression of pAKT. p58ipk suppression resulted in an increase of cell apoptosis and CHOP expression, but the expression of pAKT was significantly decreased in PQ-induced SH-SY5Y cells. However, overexpressed p58ipk led to an opposite result.
Conclusion:
The results indicated that the expression of p58ipk was related to the toxicity level of PQ-induced cells and the mechanism between them was that p58ipk regulated the toxicity might through regulating the endoplasmic reticulum stress (ER-stress) and then regulating cell apoptosis. Further studies take emphasize on the effect of ER-stress on neuron system and explore ER-stress-related therapy are important on the treatment of neurodegenerative disease.
Insights
Paraquat pesticide causes neurotoxicity by increasing cell apoptosis, linked to p58ipk and ER-stress. Understanding this mechanism may help treat neurodegenerative diseases.
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Paraquat (PQ) is a potent pesticide known to cause neurotoxicity.
- The precise pathogenic mechanisms underlying PQ-induced neurotoxicity remain unclear.
- This study aimed to elucidate the molecular pathways involved in PQ toxicity.
Purpose of the Study:
- To explore the underlying mechanism of paraquat-induced toxicity in neuronal cells.
- To investigate the role of p58ipk in paraquat toxicity.
- To identify potential therapeutic targets for neurodegenerative diseases.
Main Methods:
- Human neuroblastoma SH-SY5Y cells were treated with varying concentrations of paraquat.
- Cell apoptosis and the expression of key genes/proteins (p58ipk, CHOP, pAKT) were analyzed.
- pcDNA 3.1-p58ipk (overexpression) or si-p58ipk (suppression) was used to modulate p58ipk levels.
Main Results:
- Paraquat significantly increased cell apoptosis, p58ipk, and CHOP expression, while decreasing pAKT levels.
- Suppression of p58ipk exacerbated paraquat-induced apoptosis and CHOP expression, further reducing pAKT.
- Overexpression of p58ipk yielded opposite effects, suggesting a protective role.
Conclusions:
- p58ipk expression is directly correlated with paraquat-induced cellular toxicity.
- p58ipk may regulate paraquat toxicity by modulating endoplasmic reticulum stress (ER-stress).
- Targeting ER-stress pathways presents a potential therapeutic strategy for neurodegenerative diseases.
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