Regulation of Gonadotropin mRNA Levels in Cultured Rat Pituitary Cells by Gonadotropin-Releasing Hormone (GnRH): Role for Ca2+ and Protein Kinase C

Biochemistry ◽  
1994 ◽  
Vol 33 (12) ◽  
pp. 3698-3704 ◽  
Author(s):  
David Ben-Menahem ◽  
Zvi Naor
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Gonadotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Kinase C ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

scholarly journals Mechanism of action of gonadotropin-releasing hormone upon gonadotropin α-subunit mRNA levels in the α T3-1 cell line: role of Ca2+ and protein kinase C

1995 ◽  
Vol 309 (1) ◽  
pp. 325-329 ◽  
Author(s):  
D Ben-Menahem ◽  
Z Shraga-Levine ◽  
P L Mellon ◽  
Z Naor
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Gonadotropin Releasing Hormone ◽  
Alpha Subunit ◽  
Similar Response ◽  
Mrna Levels ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Subunit Mrna ◽  
Kinase C

Addition of [D-Trp6]gonadotropin-releasing hormone (GnRHa) to alpha T3-1 cells induced a very rapid response upon gonadotropin alpha-subunit mRNA which was detected after 30-60 min and was abolished by pretreatment with actinomycin D. A similar response was obtained with the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA), or the Ca2+ ionophore, ionomycin. GnRHa (10 nM) also stimulated a secondary rise in alpha-subunit mRNA levels between 12 and 24 h of incubation. No additivity was obtained (at 60 min) upon the combined addition of GnRHa and PMA, GnRHa and ionomycin, or PMA and ionomycin. The effect of GnRHa upon alpha-subunit mRNA was blocked by the PKC inhibitors staurosporine or GF 109203X. Down-regulation of endogenous PKC activity resulted in inhibition of the stimulatory effect of gonadotropin-releasing hormone (GnRH), PMA and ionomycin. Removal of extra-cellular Ca2+ abolished the effect of GnRHa and PMA upon alpha-subunit mRNA levels. Interestingly PMA and ionomycin had no effect on alpha-subunit mRNA levels at 24 h of incubation; however, the combined addition of the drugs mimicked the late phase of GnRHa (10 nM) action. The data provide evidence that PKC and Ca2+ are involved in mediating the early and the late responses of GnRHa upon alpha-subunit mRNA elevation and that differential cross-talk exists between the messengers.

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