N-acyl dopamines induce apoptosis in PC12 cell line via the GPR55 receptor activation
M G Akimov1, A M Ashba2, N M Gretskaya2
1Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow, 117997, Russia. akimovmike@yandex.ru.
Abstract:
Dopamine amides of arachidonic, docosahexaenoic, and oleic acids were found to induce apoptosis in PC12 cells, which was blocked exclusively by antagonists and preincubation agonists of the receptor GPR55, belonging to the group of non-CB1/CB2 receptors.
Insights
Dopamine amides of fatty acids trigger programmed cell death (apoptosis) in PC12 cells. This effect is specifically inhibited by targeting the GPR55 receptor, a non-cannabinoid receptor.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Dopamine amides are endogenous compounds with potential biological activities.
- PC12 cells are a widely used model for neuronal function and drug screening.
- The G protein-coupled receptor 55 (GPR55) is implicated in various physiological and pathological processes.
Purpose of the Study:
- To investigate the effect of dopamine amides of specific fatty acids on PC12 cell viability.
- To identify the receptor involved in mediating the cellular response to these compounds.
Main Methods:
- Treatment of PC12 cells with dopamine amides of arachidonic, docosahexaenoic, and oleic acids.
- Assessment of apoptosis induction using standard cell death assays.
- Pharmacological manipulation using GPR55 antagonists and agonists.
Main Results:
- Dopamine amides of arachidonic, docosahexaenoic, and oleic acids induced apoptosis in PC12 cells.
- GPR55 receptor antagonists and agonists blocked the apoptotic effect.
- The observed effects were specific to GPR55, as non-CB1/CB2 receptor interactions were investigated.
Conclusions:
- Dopamine amides of these fatty acids represent novel inducers of apoptosis in neuronal-like cells.
- The GPR55 receptor plays a critical role in mediating the apoptotic effects of these compounds.
- Targeting GPR55 may offer a therapeutic strategy for conditions involving excessive cell death.
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