scholarly journals Arachidonic acid and lipoxygenase products stimulate protein kinase Cβ mRNA levels in pituitary α T3-1 cell line: role in gonadotropin-releasing hormone action

1996 ◽  
Vol 316 (2) ◽  
pp. 667-670 ◽  
Author(s):  
Zurit SHRAGA-LEVINE ◽  
David BEN-MENAHEM ◽  
Zvi NAOR
Keyword(s):  
Arachidonic Acid ◽  
Protein Kinase ◽  
Cell Line ◽  
Cross Talk ◽  
Gonadotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Lipoxygenase Inhibitor ◽  
Releasing Hormone ◽  
Lipoxygenase Products

The cross-talk of arachidonic acid (AA) and its lipoxygenase products with protein kinase Cβ (PKCβ) mRNA levels during the action of gonadotropin-releasing hormone (GnRH) was investigated in the pituitary αT3-1 cell line. The addition of AA or its 5-lipoxygenase products 5-hydroxyeicosatetraenoic acid (5-HETE) or leukotriene C4 (LTC4) for 30 or 60 min stimulated PCKβ, but not PKCα mRNA levels (3–5-fold); PCKγ is not expressed by the cells. Other HETEs or leukotrienes tested showed no significant effect. The range of effective concentration for LTC4 and 5-HETE (around 10-10 M) is the range found in GnRH-stimulated pituitary cells. Although PKCβ mRNA levels were preferentially elevated by LTC4 and 5-HETE at early time points, PKCα mRNA levels were elevated at 6–12 h of incubation when PKCβ mRNA levels returned to basal levels. The addition of the phospholipase A2 inhibitor 4-bromophenacyl bromide or the selective 5-lipoxygenase inhibitor L-656,224 abolished [D-Trp6]GnRH (GnRH-A) elevation of PKCβ mRNA levels, whereas PKCα mRNA levels were not increased by this neurohormone. The cyclo-oxygenase inhibitor indomethacin elevated basal PKCβ mRNA levels and potentiated the GnRH-A response. Cross-talk exists between AA and some of its lipoxygenase products and PKCβ gene expression during cell signalling. AA, 5-HETE and LTC4 participate in the rapid stimulation of PKCβ mRNA levels by GnRH.

Protein Kinase Cδ as Gonadotropin-Releasing Hormone Target Isoenzyme in the αT3-1 Gonadotrope Cell Line

2004 ◽  
Vol 79 (4) ◽  
pp. 204-220 ◽  
Author(s):  
Hélène Maccario ◽  
Brice Junoy ◽  
Benoit Poulin ◽  
Bénédicte Boyer ◽  
Alain Enjalbert ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Line ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Protein Kinase Cδ

scholarly journals Stimulation of Jun N-Terminal Kinase (JNK) by Gonadotropin-Releasing Hormone in Pituitary αT3–1 Cell Line Is Mediated by Protein Kinase C, c-Src, and CDC42

1998 ◽  
Vol 12 (6) ◽  
pp. 815-824 ◽  
Author(s):  
Nurel L. Levi ◽  
Tamar Hanoch ◽  
Outhiriaradjou Benard ◽  
Meirav Rozenblat ◽  
Dagan Harris ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Line ◽  
Gonadotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Kinase C ◽  
Stimulation Of

PKC and ERK are differentially involved in gonadotropin-releasing hormone-induced growth hormone gene expression in the goldfish pituitary

2005 ◽  
Vol 289 (6) ◽  
pp. R1625-R1633 ◽  
Author(s):  
Christian Klausen ◽  
Takeshi Tsuchiya ◽  
John P. Chang ◽  
Hamid R. Habibi
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Primary Cultures ◽  
Gonadotropin Releasing Hormone ◽  
Growth Hormone Gene ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Gh Gene

Gonadotropin-releasing hormone (GnRH) is produced by the hypothalamus and stimulates the synthesis and secretion of gonadotropin hormones. In addition, GnRH also stimulates the production and secretion of growth hormone (GH) in some fish species and in humans with certain clinical disorders. In the goldfish pituitary, GH secretion and gene expression are regulated by two endogenous forms of GnRH known as salmon GnRH and chicken GnRH-II. It is well established that PKC mediates GnRH-stimulated GH secretion in the goldfish pituitary. In contrast, the signal transduction of GnRH-induced GH gene expression has not been elucidated in any model system. In this study, we demonstrate, for the first time, the presence of novel and atypical PKC isoforms in the pituitary of a fish. Moreover, our results indicate that conventional PKCα is present selectively in GH-producing cells. Treatment of primary cultures of dispersed goldfish pituitary cells with PKC activators (phorbol ester or diacylglycerol analog) did not affect basal or GnRH-induced GH mRNA levels, and two different inhibitors of PKC (calphostin C and GF109203X) did not reduce the effects of GnRH on GH gene expression. Together, these results suggest that, in contrast to secretion, conventional and novel PKCs are not involved in GnRH-stimulated increases in GH mRNA levels in the goldfish pituitary. Instead, PD98059 inhibited GnRH-induced GH gene expression, suggesting that the ERK signaling pathway is involved. The results presented here provide novel insights into the functional specificity of GnRH-induced signaling and the regulation of GH gene expression.

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