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Polyglutamine-containing microglia leads to disturbed differentiation and neurite retraction of neuron-like cells
Ryuji Owada1, Saaya Awata1, Kazutomo Suzue2
1Gunma University Graduate School of Health Sciences, 3-39-22, Showa-machi, Maebashi, Gunma 371-8511, Japan.
Abstract:
Expanded polyglutamine-containing proteins in neurons intrinsically contributes to neuronal dysfunctions and neuronal cell death in polyglutamine (polyQ) diseases. In addition, an expanded polyQ-containing protein in microglia also leads to apoptosis of neurons. However, detailed morphological analysis of neurons exposed to conditioned medium (CM) derived from polyQ-containing microglia has not been essentially carried out. Here, we introduced aggregated peptide with 69 glutamine repeat (69Q) into BV2 microglial cells. The 69Q-containing BV2 cells showed shorter branches. The CM from 69Q-containing microglia (69Q-CM) induced neurite retraction and fewer number of branch point of neurites of differentiated PC12 cells. Likewise, the 69Q-CM induces disturbed differentiation of PC12 cells with shorter total length of neurites and fewer number of branch point of neurites. Thus, the factor(s) released from polyQ-containing microglia affect both differentiation and degeneration of neuron-like cells.
Insights
Microglia with expanded polyglutamine (polyQ) proteins release factors that impair neuron-like cells. This study shows polyQ microglia induce neurite retraction and disrupt differentiation in PC12 cells.
Area of Science:
- Neuroscience
- Cell Biology
- Neuroinflammation
Background:
- Expanded polyglutamine (polyQ) proteins in neurons cause dysfunction and death in polyQ diseases.
- PolyQ proteins in microglia also contribute to neuronal apoptosis.
- The impact of polyQ-expressing microglia on neuronal morphology requires detailed investigation.
Purpose of the Study:
- To investigate the morphological effects of conditioned medium from polyQ-expressing microglia on neuron-like cells.
- To analyze how factors released by polyQ-laden microglia influence neuronal differentiation and neurite structure.
Main Methods:
- Aggregated peptide with 69 glutamine repeats (69Q) was introduced into BV2 microglial cells.
- Conditioned medium (CM) from 69Q-expressing BV2 cells (69Q-CM) was collected.
- Differentiated PC12 cells were exposed to 69Q-CM for morphological analysis.
Main Results:
- BV2 cells expressing 69Q exhibited reduced branching.
- 69Q-CM induced neurite retraction and decreased branching points in PC12 cells.
- 69Q-CM disrupted PC12 cell differentiation, leading to shorter neurites and fewer branch points.
Conclusions:
- Factors secreted by microglia containing expanded polyglutamine proteins negatively impact neuronal cells.
- PolyQ-expressing microglia can affect both the differentiation and degeneration of neuron-like cells.
- This highlights a potential mechanism of neurodegeneration involving microglial dysfunction in polyQ diseases.
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