Lysophosphatidylinositol Causes Neurite Retraction via GPR55, G13 and RhoA in PC12 Cells
Author Information
Author(s): Obara Yutaro, Ueno Sanae, Yanagihata Yoshimi, Nakahata Norimichi
Primary Institution: Department of Cellular Signaling, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan
Hypothesis
Does lysophosphatidylinositol (LPI) induce neurite retraction in PC12 cells through GPR55 signaling?
Conclusion
LPI promotes neurite retraction in PC12 cells via GPR55, G13, and RhoA signaling pathways, while cannabinoids do not activate GPR55 in these cells.
Supporting Evidence
- LPI increased intracellular Ca2+ concentration and RhoA activity.
- LPI caused neurite retraction in a time-dependent manner.
- LPI-induced neurite retraction was Gq-independent and G13-dependent.
- Inactivation of RhoA function prevented LPI-induced neurite retraction.
- GPR55 mRNA and protein were expressed in PC12 cells.
Takeaway
This study found that a substance called LPI makes nerve cells pull back their extensions, and it does this through a specific receptor, while other substances thought to work similarly do not.
Methodology
The study used PC12 cells to examine the effects of LPI on neurite retraction and the signaling pathways involved.
Limitations
The study primarily used a single cell line (PC12) and may not fully represent the effects in other neuronal types.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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