The Effects of CDP-Choline on Autophagy and Mitochondrial Dynamics

Kan B. , Bılge B., Bozkurt S., Ulus İ. H. , Öz Arslan D.

Second ERNEST Meeting on New Perspectives in Signal Transduction: GPCRs and Beyond, İstanbul, Turkey, 28 - 30 March 2020, pp.14

  • Publication Type: Conference Paper / Summary Text
  • City: İstanbul
  • Country: Turkey
  • Page Numbers: pp.14


The Effects of CDP-Choline on Autophagy and Mitochondrial Dynamics in Amyloid-Treated PC12 Cells #5 Beki Kan1 , Begum Bilge1 , Suleyman Bozkurt1 , Ismail Hakki Ulus2 and Devrim Oz-Arslan1 Acibadem Mehmet Ali Aydinlar University, School of Medicine, Departments of 1Biophysics and2 Medical Pharmacology, Istanbul, Turkey Section: 1. Macromolecular Interactions in Signalling Pathways, 2. Biological Roles of Signal Transduction, 3. Molecular Modulators of Signal Transduction, 4. Advanced Methodologies and Technologies 5. Public Web Resources Position of the presenter: Group leader Email address of the presenter: Recent studies suggest that autophagy may have a crucial role in Alzheimer’s disease (AD). Cytidine-5'-diphosphocholine (CDP-Ch), an intermediate in the biosynthesis of membrane phospholipids, is known to have neuroprotective effects in several diseases but the mechanism remains unclear. In this study, we aimed to understand the effect of CDP-Ch treatment on autophagy and mitochondrial dynamics during amyloid-beta (Aβ1-42) mediated neuronal injury. To this end, nerve growth factor (NGF)-differentiated PC12 cells were treated with Aβ1-42 in the presence and absence of CDP-Ch. We examined the levels of several autophagic markers, including LC3B, p62, and Beclin 1 and also Mitofusin-2 (Mfn2), an outer mitochondrial membrane GTPase involved in mitochondrial fusion by immunoblotting. Mitochondrial membrane potential (MMP) and mitochondrial mass were evaluated by flow cytometry and confocal imaging after probing with mitochondria-specific dyes. Oxygen consumption rate (OCR) was measured using Agilent Seahorse XFP Cell Mito Stress Kit. We observed increases in LCB3 and Mfn-2 levels of differentiated PC12 cells upon CDP-Ch treatment. Although CDP-Ch treatment did not cause a change in MMP, mitochondrial respiration was reduced. Aβ1-42 treatment resulted in increased levels of LC3B and Beclin 1. CDP-Ch pretreatment of injured cells reduced MitoSox levels. Our preliminary results suggest that CDP-Ch treatment and amyloid beta injury affect autophagy and mitochondrial function in NGF- differentiated PC12 cells. An understanding of the role of CDPCh in autophagy and mitochondrial dynamics may shed light into its neuroprotective effects. This work is supported by The Scientific and Technological Research Council of Turkey (Grant number:114Z494).