ATP Exists Originally in the Endoplasmic Reticulum and the organella may be the Intracellular Source of ATP Released by Stimulation of Some Receptors (pp. 197-202)
Authors: (Takeshi Katsuragi, Medical Research Center, School of Medicine, Fukuoka University, Fukuoka, Japan)
Abstract: Our research works show that ATP release induced by stimulation of G-protein
coupled receptors is regulated by two types of intracellular signaling pathways.
Stimulation of A1 receptor with adenosine, a metabolite of ATP, in MDCK cells, causes
activation of endoplasmic reticulum (ER) via Ins (1, 4, 5) P3 signal and, then
mitochondria are activated by a Ca2+-signal transducing system from ER to mitochondria.
Finally, the mitochondrial signal is transferred to some membrane devise for ATP export.
Meanwhile, stimulation of B2 receptor with bradykinin in cultured taenia coli smooth
muscle cells, activates ER via Ins (1, 4, 5) P3 stimulation and then, the ER signal is
directly delivered to some membrane devise, not to mitochondria.
Recent our study in MDCK cells demonstrated that ATP exists originally in ER.
Further, in our morphological study, ER is observed in close vicinity of the cell
membrane in smooth muscle layers.
From these findings, the author discusses here the possibility that ER may be
intracellular source of ATP released by some receptor stimulation as the latter case.