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.
Journal of Cellular Biochemistry(1996)
摘要
We investigated the early effects (5–60 s) of progesterone (1 pM–0.1 μM) on cytosolic free calcium concentration ([Ca2+]i) and inositol 1,4,5‐trisphosphate (InsP3) formation in nonluteinized and in vitro luteinized porcine granulosa cells (pGCs). Progesterone increased [Ca2+]i and InsP3 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+]i; progesterone immobilized on bovine serum albumin, which did not enter the cell, increased [Ca2+]i within 5 s and was a full agonist, but less potent than the free progesterone; pertussis toxin did not inhibit progesterone effect on InsP3. 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+]i also depends on the stage of cell luteinization. © 1996 Wiley‐Liss, Inc.
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关键词
phospholipase C,inositol-1,4,5-trisphosphate,protein kinase C,protein kinase A,progesterone
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