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Related Experiment Video

Updated: Jun 25, 2025

Neurogenesis Using P19 Embryonal Carcinoma Cells

Neurogenesis Using P19 Embryonal Carcinoma Cells

Published on: April 27, 2019

Valproic Acid Causes Redox-Regulated Post-Translational Protein Modifications That Are Dependent upon P19 Cellular

Ted B Piorczynski¹, Jouber Calixto¹, Haley C Henry¹

¹Department of Cell Biology and Physiology, Brigham Young University, Provo, UT 84602, USA.

Antioxidants (Basel, Switzerland)

|May 25, 2024

Summary

Valproic acid (VPA) causes developmental toxicity by altering protein modifications in undifferentiated cells. Activating the NRF2 antioxidant pathway protects against these effects, suggesting a way to preserve neurogenesis.

Keywords:

D3T NRF2 post-translational modifications valproic acid (VPA)

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Last Updated: Jun 25, 2025

Neurogenesis Using P19 Embryonal Carcinoma Cells

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Published on: April 27, 2019

Fluorescence-based Monitoring of PAD4 Activity via a Pro-fluorescence Substrate Analog

Fluorescence-based Monitoring of PAD4 Activity via a Pro-fluorescence Substrate Analog

Published on: November 5, 2014

Utilizing a Comprehensive Immunoprecipitation Enrichment System to Identify an Endogenous Post-translational Modification Profile for Target Proteins

Published on: January 8, 2018

Area of Science:

Neuroscience
Toxicology
Biochemistry

Background:

Valproic acid (VPA) is an anti-epileptic drug with known neurodevelopmental toxicity.
VPA disrupts redox signaling in undifferentiated cells, but not in differentiated neurons.
Redox imbalances can alter protein modifications, potentially impacting embryogenesis.

Purpose of the Study:

To investigate if VPA causes redox-sensitive post-translational protein modifications.
To determine if these modifications are dependent on cellular differentiation state.
To explore the role of the NRF2 antioxidant pathway in mitigating VPA toxicity.

Main Methods:

P19 cells and P19-derived neurons were treated with VPA.
Some cells were pretreated with D3T, an inducer of the NRF2 pathway.
Analyzed redox balance (glutathione couple) and protein oxidation levels.

Main Results:

Undifferentiated cells showed an oxidized glutathione redox couple and increased protein oxidation after VPA exposure.
Differentiated neurons were protected from protein oxidation by increased S-glutathionylation.
D3T pretreatment prevented VPA's adverse effects in undifferentiated cells.

Conclusions:

VPA-induced developmental toxicity may stem from redox-sensitive protein alterations in undifferentiated cells.
NRF2 pathway activation offers a protective mechanism against VPA's effects.
Targeting NRF2 could be a strategy to maintain neurogenesis during VPA exposure.