Arachidonic acid and Lipoxygenase Products Stimulate Gonadotropin .alpha.-Subunit mRNA Levels in Pituitary .alpha.T3-1 Cell Line: Role in Gonadotropin Releasing Hormone Action

Biochemistry ◽  
1994 ◽  
Vol 33 (43) ◽  
pp. 12795-12799 ◽  
Author(s):  
David Ben-Menahem ◽  
Zurit Shraga-Levine ◽  
Rona Limor ◽  
Zvi Naor
Keyword(s):  
Arachidonic Acid ◽  
Cell Line ◽  
Gonadotropin Releasing Hormone ◽  
Alpha Subunit ◽  
Mrna Levels ◽  
Hormone Action ◽  
Releasing Hormone ◽  
Subunit Mrna ◽  
Lipoxygenase Products

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.

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.

Hypothalamic Thyrotropin-Releasing Hormone Regulates Pituitary Thyrotropin Beta- and Alpha-Subunit mRNA Levels in the Rat

1991 ◽  
Vol 53 (3) ◽  
pp. 276-280 ◽  
Author(s):  
Masami Murakami ◽  
Masatomo Mori ◽  
Yukio Kato ◽  
Isao Kobayashi
Keyword(s):  
Thyrotropin Releasing Hormone ◽  
Alpha Subunit ◽  
Mrna Levels ◽  
Releasing Hormone ◽  
Subunit Mrna

Desensitization of gonadotropin-releasing hormone action in the gonadotrope-derived alpha T3-1 cell line.

Endocrinology ◽  
1995 ◽  
Vol 136 (11) ◽  
pp. 4864-4871 ◽  
Author(s):  
C A McArdle ◽  
W Forrest-Owen ◽  
G Willars ◽  
J Davidson ◽  
A Poch ◽  
...  
Keyword(s):  
Cell Line ◽  
Gonadotropin Releasing Hormone ◽  
Hormone Action ◽  
Releasing Hormone

Dissociation between release and gene expression of gonadotropin .alpha.-subunit in gonadotropin-releasing hormone-stimulated .alpha.T3-1 cell line

Biochemistry ◽  
1992 ◽  
Vol 31 (51) ◽  
pp. 12893-12898 ◽  
Author(s):  
David Ben-Menahem ◽  
Zurit Shraga ◽  
Hadas Lewy ◽  
Rona Limor ◽  
Ilan Hammel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Gonadotropin Releasing Hormone ◽  
Alpha Subunit ◽  
Releasing Hormone

Role of PKC in the regulation of gonadotropin subunit mRNA levels: interaction with two native forms of gonadotropin-releasing hormone

2005 ◽  
Vol 289 (6) ◽  
pp. R1634-R1643 ◽  
Author(s):  
Christian Klausen ◽  
David L. Severson ◽  
John P. Chang ◽  
Hamid R. Habibi
Keyword(s):  
Primary Cultures ◽  
Gonadotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Releasing Hormone ◽  
Subunit Mrna ◽  
Important Regulator ◽  
Lh Secretion

Gonadotropin-releasing hormone (GnRH) is an important regulator of reproduction in all vertebrates through its actions on the production and secretion of pituitary gonadotropin hormones (GtHs). Most vertebrate species express at least two GnRHs, including one form, designated chicken (c)GnRH-II or type II GnRH, which has been well conserved throughout evolution. The goldfish brain and pituitary contain salmon GnRH and cGnRH-II. In goldfish, GnRH-induced luteinizing hormone (LH) secretion involves PKC; however, whether PKC mediates GnRH stimulation of GtH subunit mRNA levels is unknown. In this study, we used inhibitors and activators of PKC to examine its possible involvement in GnRH-induced increases in GtH-α, follicle-stimulating hormone (FSH)-β and LH-β mRNA levels in primary cultures of dispersed goldfish pituitary cells. Treatment with PKC inhibitors calphostin C and GF109203X unmasked a basal repression of GtH subunit mRNA levels by PKC; both inhibitors increased GtH subunit mRNA levels in a dose-dependent manner. PKC activators, 12- O-tetradecanoylphorbol 13-acetate (TPA), and 1,2-dioctanoyl- sn-glycerol, stimulated GtH subunit mRNA levels, whereas an inactive phorbol ester (4-α-TPA) was without effect. Thus, a dual, inhibitory and stimulatory, influence for PKC in the regulation of GtH subunit mRNA levels is suggested. In contrast, PKC inhibitor- and activator-induced effects were, for the most part, additive to those of GnRH, suggesting that conventional and novel PKCs are unlikely to be involved in GnRH-stimulated increases in GtH subunit mRNA levels. Our data illustrate major differences in the signal transduction of GnRH effects on GtH secretion and gene expression in the goldfish pituitary.

scholarly journals Desensitization of Gonadotropin-releasing Hormone Action in αT3-1 Cells Due to Uncoupling of Inositol 1,4,5-Trisphosphate Generation and Ca2+Mobilization

1996 ◽  
Vol 271 (39) ◽  
pp. 23711-23717 ◽  
Author(s):  
Craig A. McArdle ◽  
Gary B. Willars ◽  
Robert C. Fowkes ◽  
Stefan R. Nahorski ◽  
James S. Davidson ◽  
...  
Keyword(s):  
Gonadotropin Releasing Hormone ◽  
Hormone Action ◽  
Releasing Hormone ◽  
Inositol 1,4,5 Trisphosphate
Sign in / Sign up

Export Citation Format

Share Document