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PTPRR regulates ERK dephosphorylation in depression mice model
Xinrong Li1, Zhifen Liu1, Wei Li1
1Department of Psychiatry, First Hospital of Shanxi Medical University, Taiyuan, China.
Journal of Affective Disorders
|January 17, 2016
Summary
Overexpressing Protein tyrosine phosphatase receptor type R (PTPRR) in the hippocampus increases depression-like behaviors and stress sensitivity by affecting MAPK signaling. Targeting the PTPRR/ERK pathway may offer new depression therapies.
Area of Science:
- Neuroscience
- Molecular Biology
- Psychiatry
Background:
- Protein tyrosine phosphatase receptor type R (PTPRR) regulates mitogen-activated protein kinase (MAPK) signaling, impacting cell proliferation, apoptosis, and synaptic plasticity.
- Dysregulation of PTPRR may contribute to the pathogenesis of depression.
Purpose of the Study:
- To investigate the role of PTPRR in the hippocampal dentate gyrus (DG) in depression-like behaviors.
- To explore the effects of PTPRR manipulation on MAPK signaling, neuronal apoptosis, and cell proliferation in the context of chronic mild stress (CMS).
Main Methods:
- Lentiviral vectors were used to overexpress or inhibit PTPRR in the mouse hippocampal DG.
- Behavioral tests (forced swim, tail suspension, sucrose preference) were conducted.
- MAPK (ERK, P38) phosphorylation, neuronal apoptosis (TUNEL assay), and cell proliferation (BrdU incorporation) were assessed.
Main Results:
- PTPRR overexpression induced depression-like behaviors and increased sensitivity to CMS.
- PTPRR manipulation altered ERK and P38 phosphorylation levels.
- PTPRR overexpression led to increased neuronal apoptosis and decreased cell proliferation in the DG, with or without CMS.
Conclusions:
- PTPRR overexpression in the hippocampal DG promotes depression onset and exacerbates stress sensitivity via ERK dephosphorylation.
- The PTPRR/ERK pathway is implicated in neuronal apoptosis and reduced cell proliferation.
- The PTPRR/ERK pathway represents a potential therapeutic target for depression.
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