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

Klausen, Christian; Severson, David L.; Chang, John P.; Habibi, Hamid R.

doi:10.1152/ajpregu.00186.2005

Cited by 15 publications

(9 citation statements)

References 54 publications

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“…A similar finding with differential involvement of PKC in pituitary adenylate cyclaseactivating peptide-induced SL␣ and SL␤ expression via PLC-dependent mechanisms has been recently reported in the carp pituitary (47). Given that multiple isoforms of PKC have been identified in the fish pituitary, eg, goldfish (48), and some of them, eg, PKC and PKC , are known to have atypical pharmacological properties (49), we do not exclude the possibility that PKC isoforms insensitive to GF109203X might be involved in the PRL responses occurred in the carp pituitary. In our study, Ca 2ϩ imaging also revealed that NKB and NKBRP were both effective in triggering a biphasic Ca 2ϩ rise with an initial peak followed by a shoulder phase in carp pituitary cells.…”

Section: Discussionsupporting

confidence: 80%

Novel Pituitary Actions of TAC3 Gene Products in Fish Model: Receptor Specificity and Signal Transduction for Prolactin and Somatolactin α Regulation by Neurokinin B (NKB) and NKB-Related Peptide in Carp Pituitary Cells

et al. 2014

Endocrinology

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TAC3 is a member of tachykinins, and its gene product neurokinin B (NKB) has recently emerged as a key regulator for LH through modulation of kisspeptin/GnRH system within the hypothalamus. In fish models, TAC3 not only encodes NKB but also a novel tachykinin-like peptide called NKB-related peptide (NKBRP), and the pituitary actions of these TAC3 gene products are still unknown. Using grass carp as a model, the direct effects and postreceptor signaling for the 2 TAC3 products were examined at the pituitary level. Grass carp TAC3 was cloned and confirmed to encode NKB and NKBRP similar to that of other fish species. In carp pituitary cells, NKB and NKBRP treatment did not affect LH release and gene expression but up-regulated prolactin (PRL) and somatolactin (SL)α secretion, protein production, and transcript expression. The stimulation by these 2 TAC3 gene products on PRL and SLα release and mRNA levels were mediated by pituitary NK2 and NK3 receptors, respectively. Apparently, NKB- and NKBRP-induced SLα secretion and transcript expression were caused by adenylate cyclase/cAMP/protein kinase A, phospholipase C/inositol 1,4,5-triphosphate/protein kinase C and Ca(2+)/calmodulin/Ca(2+)/calmodulin-dependent protein kinase II activation. The signal transduction for the corresponding responses on PRL release and mRNA expression were also similar, except that the protein kinase C component was not involved. These findings suggest that the 2 TAC3 gene products do not play a role in LH regulation at the pituitary level in carp species but may serve as novel stimulators for PRL and SLα synthesis and secretion via overlapping postreceptor signaling mechanisms coupled to NK2 and NK3 receptors, respectively.

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Section: Discussionsupporting

confidence: 80%

Novel Pituitary Actions of TAC3 Gene Products in Fish Model: Receptor Specificity and Signal Transduction for Prolactin and Somatolactin α Regulation by Neurokinin B (NKB) and NKB-Related Peptide in Carp Pituitary Cells

et al. 2014

Endocrinology

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“…These results argue against the possibility that TPA-induced SL gene expression was caused by PKC desensitization. This idea was also supported by the studies using DiC8 (10 M), a nondesensitizing diacylglycerol analog (17) that could mimic TPA stimulation of SL␣ and SL␤ mRNA expression in carp pituitary cells (Fig. 4B, inset).…”

Section: Pacap Induction Of Sl␣ and Sl␤ Mrna Expressionmentioning

confidence: 59%

“…Despite the fact that the rise in SL␤ mRNA levels caused by PACAP could be negated by inhibiting PLC and IP 3 receptors, this stimulatory action was not affected by PKC blockade, suggesting that the PKC component may be uncoupled from PLC-dependent mechanisms leading to SL␤ gene expression. Since PKC isoforms are expressed in the goldfish pituitary in a cell-type specific manner (17) and the atypical isoforms, e.g., PKC and PKC , are known to be insensitive to stimulation by phorbol ester and diacylglycerol (25), it is tempting to speculate that the lack of PKC involvement in PACAP-induced SL␤ (14). These findings raise the possibility that the Ca 2ϩ /CaM-dependent cascades for SL gene expression may be secondarily coupled with the PKA-and PKC-dependent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Grass carp somatolactin: II. Pharmacological study on postreceptor signaling mechanisms for PACAP-induced somatolactin-α and -β gene expression

Jiang

He²,

Wang³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Somatolactin (SL), the latest member of the growth hormone/prolactin family, is a novel pituitary hormone with diverse functions. However, the signal transduction mechanisms responsible for SL expression are still largely unknown. Using grass carp as an animal model, we examined the direct effects of pituitary adenylate cyclase-activating polypeptide (PACAP) on SL gene expression at the pituitary level. In primary cultures of grass carp pituitary cells, SL␣ and SL␤ mRNA levels could be elevated by PACAP via activation of PAC-I receptors. With the use of a pharmacological approach, the AC/cAMP/PKA and PLC/inositol 1,4,5-trisphosphate (IP 3)/PKC pathways and subsequent activation of the Ca 2ϩ /calmodulin (CaM)/CaMK-II cascades were shown to be involved in PACAP-induced SL␣ mRNA expression. Apparently, the downstream Ca 2ϩ /CaM-dependent cascades were triggered by extracellular Ca 2ϩ ([Ca 2ϩ ]e) entry via L-type voltagesensitive Ca 2ϩ channels (VSCC) and Ca 2ϩ release from IP3-sensitive intracellular Ca 2ϩ stores. In addition, the VSCC component could be activated by cAMP/PKA-and PLC/PKC-dependent mechanisms. Similar postreceptor signaling cascades were also observed for PACAP-induced SL␤ mRNA expression, except that [Ca 2ϩ ]e entry through VSCC, PKC coupling to PLC, and subsequent activation of CaMK-II were not involved. These findings, taken together, provide evidence for the first time that PACAP can induce SL␣ and SL␤ gene expression in fish model via PAC-I receptors through differential coupling to overlapping and yet distinct signaling pathways.pituitary adenylate cyclase-activating polypeptide; grass carp pituitary cells SOMATOLACTIN (SL), the latest member of the growth hormone (GH)/prolactin (PRL) family, can be identified only in fish but not in tetrapods (37). Phylogenetic analysis reveals that SL is derived from ancestral GH (16), and gene duplication in bony fish have given rise to two paralogous SL isoforms, namely SL␣ and SL␤ (47). Unlike GH and PRL, which are nonglycosylated and expressed mainly in the anterior pituitary, SL is a glycoprotein secreted by the periodic acid Schiff-positive cells located in the pars intermedia (15). Although the physiological functions of SL have not been fully characterized, its involvement in color presentation (7), body metabolism (8), osmoregulation (18), stress responses (30), and reproductive functions (31) has been proposed by various studies in fish models. Recently, it has been shown that swim bladder development can be inhibited in zebrafish by SL␤ but not SL␣ gene silencing, implying that the two SL isoforms may act differently during the process of embryo organogenesis (46). In rainbow trout, SL release can be suppressed by dopamine but stimulated by corticotropin-releasing hormone and gonadotropin-releasing hormone (GnRH; Ref. 13). In addition, SL mRNA expression can be upregulated by GnRH treatment (e.g., salmon; Ref. 26), which is in agreement with the previous reports (28) that GnRH receptors are expressed in fish pituitary cells with SL immunoreact...

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“…Despite the fact that the reduction in SL␤ mRNA levels caused by gbSS-28 could be negated by inhibiting PLC and IP 3 receptors, this inhibitory action was not affected by PKC blockade, suggesting that the PKC component may be uncoupled from PLC-dependent mechanisms leading to SL␤ gene expression. Because PKC isoforms are expressed in the goldfish pituitary in a cell type-specific manner (22), the differential regulation of the SL isoforms may result from different components of PKC isoforms expressed in NIL cells. Also, given that IP 3 receptors are Ca 2ϩ channels responsible for intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) release from IP 3 -sensitive Ca 2ϩ stores (11), we should not rule out the possibility that [Ca 2ϩ ] i mobilization may contribute to gbSS-28-inhibited SL gene expression.…”

Section: R764mentioning

confidence: 99%

Somatostatin-28 inhibitory action on somatolactin-α and -β gene expression in goldfish

Jiang

Wong

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Somatostain (SS) is known to inhibit growth hormone (GH) and prolactin (PRL) secretion. Somatolactin (SL) is a member of the GH/PRL family, but its regulation by goldfish brain somatostatin-28 (gbSS-28) has not been examined. To this end, the structural identity of goldfish SLα was established by 5'/3'-rapid amplification of cDNA ends. As revealed by in situ hybridization and immunohistochemical staining, the expression of SL isoforms was detected in pituitary cells located in the neurointermediate lobe (NIL). The transcripts of goldfish SS receptor 5a (Sst5a) but not Sst1b, Sst2, or Sst3a were detected in the goldfish NIL cells by RT-PCR. In goldfish pituitary cells, gbSS-28 not only had an inhibitory effect on basal SLα and SLβ mRNA levels but also could abolish insulin-like growth factor-stimulated SL gene expression. In primary cultures of goldfish NIL cells, gbSS-28 reduced forskolin-stimulated total cAMP production. With the use of a pharmacological approach, the adenylate cyclase (AC)/cAMP and phospholipase C (PLC)/inositol trisphosphate (IP3)/protein kinase C (PKC) cascades were shown to be involved in gbSS-28-inhibited SLα mRNA expression. Similar postreceptor signaling cascades were also observed for gbSS-28-reduced SLβ mRNA expression, except that PKC coupling to PLC was not involved. These results provide evidence that gbSS-28 can inhibit SLα and SLβ gene expression at the goldfish pituitary level via Sst5 through differential coupling of AC/cAMP and PLC/IP3/PKC cascades.

show abstract

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

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

Cited by 15 publications

References 54 publications

Novel Pituitary Actions of TAC3 Gene Products in Fish Model: Receptor Specificity and Signal Transduction for Prolactin and Somatolactin α Regulation by Neurokinin B (NKB) and NKB-Related Peptide in Carp Pituitary Cells

Novel Pituitary Actions of TAC3 Gene Products in Fish Model: Receptor Specificity and Signal Transduction for Prolactin and Somatolactin α Regulation by Neurokinin B (NKB) and NKB-Related Peptide in Carp Pituitary Cells

Grass carp somatolactin: II. Pharmacological study on postreceptor signaling mechanisms for PACAP-induced somatolactin-α and -β gene expression

Somatostatin-28 inhibitory action on somatolactin-α and -β gene expression in goldfish

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