Prostaglandin F 2α potentiates the calcium dependent activation of mitochondrial metabolism in luteal cells

Abstract

Cytoplasmic Ca 2+ signals are transferred to the mitochondria and activate the Krebs cycle. We have compared the efficiency of this process for two Ca 2+ mobilising agonists, PGF 2α and ATP (acting at metabotropic P 2 receptors) in rat luteal cells. [Ca 2+] c, [Ca 2+] m and mitochondrial NAD(P)H were monitored by means of microspectrofluorimetry and confocal microscopy. While both agonists caused similar elevations of [Ca 2+] c, changes in NAD(P)H were larger in response to PGF 2α than to ATP. PGF 2α more effectively increased NAD(P)H level also in mouse luteal cells. PGF 2α caused a faster rate of rise of NAD(P)H fluorescence than ATP when reoxidation was prevented with rotenone, suggesting a faster rate of NAD(P) + reduction. The NAD(P)H response to both agonists was dependent on the mobilisation of stored Ca 2+. We found no difference in the efficacy of transmission of the [Ca 2+] c signal to mitochondria in response to PGF 2α and ATP. Raising [Ca 2+] c with ionomycin increased the NAD(P)H signal, which was further raised by PGF 2α but not by ATP. These data suggest that PGF 2α potentiates the Ca 2+-induced stimulation of mitochondrial metabolism by a Ca 2+-independent mechanism and shows that agonists may modulate mitochondrial function differentially through a novel process beyond the simple transfer of Ca 2+ from ER to mitochondria.