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.

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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