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Updated: Jun 22, 2026
An Improved Protocol to Purify and Directly Mono-Biotinylate Recombinant BDNF in a Tube for Cellular Trafficking Studies in Neurons
Published on: July 11, 2020
[MPP+ decreased BDNF expression in PC12 cells]
Yu-he Yuan1, Jian-dong Sun, Jin-feng Hu
1Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
Abstract:
The aim of this study is to investigate the neurotoxic effect and mechanism of 1-methyl-4-phenylpyridinium (MPP+) on PC12 cells. MTT assay was used to investigate cell viability, Western blotting assay was performed to observe the protein level and phosphorylation, and dual-luciferase assay was used to study the transactivation. The experiment showed that MPP+ could decrease cell viability significantly in a dose-dependent manner and could decrease BDNF protein level, depress the phosphorylation of ERK, and attenuate the phosphorylation and transactivation of CREB, which is one of transcription factors of BDNF, but did not affect the activity of CaMK II in PC12 cells. So MPP+ might decrease BDNF protein level through MAPK/ERK signal pathway.
Insights
1-methyl-4-phenylpyridinium (MPP+) reduces PC12 cell viability and brain-derived neurotrophic factor (BDNF) levels by inhibiting the MAPK/ERK pathway and CREB phosphorylation.
Area of Science:
- Neuroscience
- Cell Biology
- Molecular Biology
Context:
- 1-methyl-4-phenylpyridinium (MPP+) is a neurotoxin implicated in Parkinson's disease research.
- PC12 cells are a widely used cell line for studying neuronal function and toxicity.
- Understanding the molecular mechanisms of neurotoxicity is crucial for developing therapeutic strategies.
Purpose:
- To elucidate the neurotoxic effects of MPP+ on PC12 cells.
- To investigate the underlying molecular mechanisms, including effects on cell viability, protein levels, and signaling pathways.
Summary:
- MPP+ significantly decreased PC12 cell viability in a dose-dependent manner.
- MPP+ reduced brain-derived neurotrophic factor (BDNF) protein levels.
- MPP+ inhibited the phosphorylation of ERK and the phosphorylation/transactivation of CREB, a key transcription factor for BDNF, via the MAPK/ERK pathway, without affecting CaMK II activity.
Impact:
- Identifies the MAPK/ERK signaling pathway and CREB as critical mediators in MPP+-induced neurotoxicity.
- Provides insights into the molecular basis of BDNF downregulation by MPP+.
- Contributes to the understanding of neurodegenerative processes and potential therapeutic targets.
