Abstract
Nicotinic acetylcholine receptors (nAChRs) regulate mitochondria-driven apoptosis; however, their intracellular ligands are unknown. In the present paper, we show that choline and its derivatives (phosphocholine (PC), L-α-glycerophosphocholine (G-PC) and 1-palmitoyl-sn-glycero-3-phosphocholine (P-GPC)) dose-dependently influence cytochrome c release from isolated mouse liver mitochondria. Choline inhibited Ca2+-stimulated cytochrome c release, while PC attenuated wortmannin-induced cytochrome c release. Small doses of G-PC and P-GPC (up to 0.1 µM) were protective against either Ca2+ or wortmannin, while larger doses (up to 1 µM) stimulated cytochrome c release by themselves. Choline and PC disrupted interaction of VDAC1, Bax and Bcl-2 with mitochondrial α7 nAChRs and favored their interaction with α9 nAChR subunits. It is concluded that choline metabolites can regulate apoptosis by affecting mitochondrial nAChRs. Keywords: apoptosis, choline, choline derivatives, cytochrome c, mitochondria, nicotinic acetylcholine receptor
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
