Extracellular signal-regulated kinase mediates gonadotropin subunit gene expression and LH release responses to endogenous gonadotropin-releasing hormones in goldfish

Klausen, Christian; Booth, Morgan; Habibi, Hamid R.; Chang, John P.

doi:10.1016/j.ygcen.2008.05.003

Cited by 19 publications

(9 citation statements)

References 59 publications

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“…In fish, studies with tilapia (Yaron et al, ) and a‐T3‐1 cells expressing the Chinook salmon LH gene (Ando & Urano, ) showed that GnRH increases LH mRNA via PKC‐mediated activation of ERK. However, in goldfish pituitary cells, PKC does not mediate GnRH action on GTH gene expression via ERK (Klausen, Booth, Habibi, & Chang, ; Klausen, Chang, & Habibi, , ; Klausen, Severson, Chang, & Habibi, ). In the present study, the gene expression of ERK2 showed a similar trend with serum GnRH concentration in response to dietary ARA, and ARA supplementation also increased the gene expression of PKCβ (but not that of PKCα).…”

Section: Discussionmentioning

confidence: 99%

Possible involvement of PKC/MAPK pathway in the regulation of GnRH by dietary arachidonic acid in the brain of male tongue sole Cynoglossus semilaevis

Sun

Liao

et al. 2019

Aquac Res

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Our previous studies have indicated that dietary arachidonic acid (ARA) significantly affects the gonadal steroidogenesis in the marine teleost tongue sole Cynoglossus semilaevis, and this effect was more positive in male fish than in female fish (Aquaculture, 468,(378)(379)(380)(381)(382)(383)(384)(385). As a following up study, the present study was further aimed at investigating the possible mechanisms in the brain mediating the effects of dietary ARA on gonadal steroidogenesis. A 70-day feed trial was repeated with two-year-old tongue sole, using three experimental diets with graded levels of ARA, 0.34%, 2.53%, and 9.63% of total fatty acids. Each diet was fed to triplicate groups of 23 fish (15 males and 8 females). The results confirmed the positive effect of dietary ARA on testosterone production in male fish. The concentration of gonadotrophin-releasing hormone (GnRH) in serum responded to dietary ARA in a similar pattern with the testosterone concentration, but the concentration of gonadotrophin in serum was not affected by dietary ARA. The response of gene expression of PKCβ, ARRB1, ARRB2, ERK2 and ATF3 in the brain to dietary ARA was in good agreement with those of GnRH and testosterone, indicating the possible involvement of PKC-ARRB-ERK-ATF3 pathway in signalling transduction of GnRH. However, the PI3K/Akt and TLR/NF-κB pathways may not be directly involved in the regulation of GnRH metabolism by ARA. This is the first study reporting the possible involvement of PKC/MAPK pathways in regulation of reproductive endocrine processes by long-chain polyunsaturated fatty acid in brain of marine fish. K E Y W O R D Sarachidonic acid, brain, Cynoglossus semilaevis, PKC/MAPK, reproduction Abbreviations: 3β-HSD, 3β-hydroxysteroid dehydrogenase; Akt1, protein kinase B 1; ARA, arachidonic acid; ARRB, arrestin beta; ATF3, activating transcription factor 3; CREB, cAMP responsive element binding protein; DHA, docosahexaenoic acid; ELISA, enzyme-linked immunosorbent assay; EPA, eicosapentaenoic acid; ERK, extracellular-regulated protein kinase;

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Section: Discussionmentioning

confidence: 99%

Possible involvement of PKC/MAPK pathway in the regulation of GnRH by dietary arachidonic acid in the brain of male tongue sole Cynoglossus semilaevis

Sun

Liao

et al. 2019

Aquac Res

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“…The MAPK3/1 pathway mediates, at least in part, GnRHinduced gonadotropin subunit gene expression [6,25,30].…”

Section: Discussionmentioning

confidence: 99%

“…GnRH-induced activation of MAPK3/1 is known to be involved in gonadotropin subunit gene expression [5][6][7][8]. MAP3K1, a kinase upstream of MAPK3/1 in the MAPK pathway, exerts its effect on the downstream MAPK3/1.…”

Section: Effect Of Dusp1 Overexpression On Map3k1-activated Gonadotromentioning

confidence: 99%

“…PKC ultimately activates mitogen-activated protein kinase 3/1 (MAPK3/1), a member of the mitogen-activated protein kinase (MAPK) family [4]. Activation of MAPK family proteins such as MAPK3/1, c-Jun N-terminal kinase, p38 MAPK, and MAPK7 has been reported to mediate GnRH-induced gonadotropin subunit expression [5][6][7][8][9]. GnRH also couples with Gs protein to increase cAMP accumulation [10].…”

Section: Introductionmentioning

confidence: 99%

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Induction of Dual-Specificity Phosphatase 1 (DUSP1) by Pulsatile Gonadotropin-Releasing Hormone Stimulation: Role for Gonadotropin Subunit Expression in Mouse Pituitary LbetaT2 Cells1

Purwana

Kanasaki

Mijiddorj

et al. 2011

Biology of Reproduction

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In pituitary gonadotrophs, GnRH induces expression of the mitogen-activated protein kinases (MAPK3/1) dephosphorylating enzyme, dual-specificity phosphatase 1 (DUSP1). Here we examined DUSP1 expression levels following pulsatile GnRH stimulation of the LbetaT2 gonadotroph cells. DUSP1 expression was increased more prominently following high-frequency (every 30 min) GnRH pulse stimulation (7.02- ± 1.47-fold) than low-frequency (every 120 min) GnRH pulses (2.68- ± 0.09-fold). With high-frequency GnRH pulses, DUSP1 expression increased by 2.89- ± 0.32-fold 2 h after GnRH pulse initiation (four 5-min pulses). DUSP1 expression was not induced following lower frequency GnRH pulses, even when the GnRH concentration was increased. Under high-frequency conditions, MAPK3/1 phosphorylation was observed 10 min after the GnRH pulse and decreased to basal levels after 25 min. However, MAPK3/1 dephosphorylation did not occur concurrently with DUSP1 expression. Overexpression of MAP3K1, a kinase upstream of MAPK3/1, increased both the Lhb and the Fshb subunit promoter activities, which could be completely inhibited by cotransfection with DUSP1-expressing vectors. Serum response factor (Srf) promoter activities induced by MAP3K1 were also prevented by DUSP1 overexpression, confirming that MAPK3/1 has an important role in gonadotropin subunit gene expression. Both high- and low-frequency GnRH pulse stimulation failed to increase the Lhb and Fshb subunit gonadotropin gene expression levels upon DUSP1 overexpression. Our study demonstrates that DUSP1 is specifically expressed following high-frequency GnRH pulses and that this effect may participate in the differential regulation of gonadotropin subunit expression in association with MAPK3/1 phosphorylation.

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“…The lack of a change in the GnRH‐induced Ca 2+ signal in somatotrophs, whereas the GH release response is reduced, also raises the possibility that PI3K mediation of sGnRH GH release occurs at transduction steps distal to (or not directly related to) sGnRH‐induced Ca 2+ signal generation. sGnRH post‐receptor signalling leading to stimulation of GH secretion in goldfish also involves the activation of PKC and mitogen‐activated protein kinase (MAPK; especially extracellular signal‐related kinase) (60). PI3K is known to target PKC and MAPK.…”

Section: Discussionmentioning

confidence: 99%

Differential Involvement of Phosphoinositide 3-Kinase in Gonadotrophin-Releasing Hormone Actions in Gonadotrophs and Somatotrophs of Goldfish, Carassius auratus

Pemberton

Stafford

et al. 2011

Journal of Neuroendocrinology

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In goldfish, two endogenous gonadotrophin-releasing hormones (GnRHs) [salmon (s)GnRH and chicken (c)GnRH-II] control maturational gonadotrophin-II [lutenising hormone (LH)] and growth hormone (GH) secretion via Ca(2+)-dependent intracellular signalling pathways. We investigated the involvement of phosphoinositide 3-kinase (PI3K) in GnRH-evoked LH and GH release and associated intracellular Ca(2+) increases ([Ca(2+)](i) ) in goldfish gonadotrophs and somatotrophs. Immunoreactive PI3K p85α, the predominant regulatory subunit for class IA PI3Ks, was detected in goldfish pituitary tissue extracts and both endogenous GnRH isoforms increased phosphorylation of PI3K p85α in excised pituitary fragments. sGnRH- and cGnRH-II-elicited LH release responses from primary cultures of pituitary cells and [Ca(2+)](i) increases in identified gonadotrophs were significantly reduced in the presence of PI3K inhibitors wortmannin (100 nm) and LY294002 (10 μm). Unexpectedly, wortmannin and LY294002 inhibited GnRH-evoked GH release but only attenuated the [Ca(2+)](i) response in identified somatotrophs to cGnRH-II, and not sGnRH. On the other hand, Ca(2+) ionophore-evoked LH and GH secretion remained unaltered in the presence of the PI3K inhibitors, suggesting that general decreases in the releasable hormone pool or sensitivity to [Ca(2+)](i) changes did not underlie the ability of wortmannin and LY294002 to reduce the actions of GnRH. These results provide the first evidence for the presence and involvement of PI3K in GnRH-induced LH and GH release in any primary pituitary cell system. In gonadotrophs, the inhibitory action of PI3K on both sGnRH and cGnRH-II involves the attenuation of their evoked [Ca(2+)](i); in contrast, GnRH isoform-specific effects occur in somatotrophs.

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Extracellular signal-regulated kinase mediates gonadotropin subunit gene expression and LH release responses to endogenous gonadotropin-releasing hormones in goldfish

Cited by 19 publications

References 59 publications

Possible involvement of PKC/MAPK pathway in the regulation of GnRH by dietary arachidonic acid in the brain of male tongue sole Cynoglossus semilaevis

Possible involvement of PKC/MAPK pathway in the regulation of GnRH by dietary arachidonic acid in the brain of male tongue sole Cynoglossus semilaevis

Induction of Dual-Specificity Phosphatase 1 (DUSP1) by Pulsatile Gonadotropin-Releasing Hormone Stimulation: Role for Gonadotropin Subunit Expression in Mouse Pituitary LbetaT2 Cells1

Differential Involvement of Phosphoinositide 3-Kinase in Gonadotrophin-Releasing Hormone Actions in Gonadotrophs and Somatotrophs of Goldfish, Carassius auratus

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