Progesterone triggers rapid transmembrane calcium influx and/or calcium mobilization from endoplasmic reticulum, via a pertussis-insensitive G-protein in granulosa cells in relation to luteinization process
✍ Scribed by Véronique Machelon; Françoise Nomé; Brigitte Grosse; Michèle Lieberherr
- Book ID
- 102655858
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 915 KB
- Volume
- 61
- Category
- Article
- ISSN
- 0730-2312
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✦ Synopsis
We investigated the early effects (5-60 s) of progesterone (1 pM-0.1 pM) on cytosolic free calcium concentration ([Ca2+l,) and inositol 1,4,5-trisphosphate (InsP3) formation in nonluteinized and in vitro luteinized porcine granulosa cells (pGCs). Progesterone increased [Ca2+l, and InsP, formation within 5 s in both cell types.
Progesterone induced calcium mobilization from the endoplasmic reticulum via the activation of a phospholipase C linked to a pertussis-insensitive G-protein. This process was controlled by protein kinases C and A. In contrast, only nonluteinized pGCs showed a Ca2+ influx via dihydropyridine-insensitive calcium channel. In both cell types, the nuclear progesterone receptor antagonist RU-38486 did not inhibit the progesterone-induced increase in [Ca2+],; progesterone immobilized on bovine serum albumin, which did not enter the cell, increased [Ca2+], within 5 sand was a full agonist, but less potent than the free progesterone; pertussis toxin did not inhibit progesterone effect on InsP,. In conclusion, progesterone may interact with membrane unconventional receptors that belong to the class of membrane receptors coupled to a phospholipase C via a pertussis toxin-insensitive G-protein. The source of the Ca2+ for the progesterone-induced increase in [Ca2+], also depends on the stage of cell luteinization. P 1996 Wiley-Liss, Inc