Abstract

In our previous study, NKB/NK3R system has been shown to act at the pituitary level to up-regulate SLα synthesis and secretion in grass carp. However, whether NK3R expression can serve as a regulatory target at the pituitary level and contribute to NKB interactions with other SLα regulators is still unclear. In current study, using grass carp pituitary cells as a model, we have a novel finding that co-treatment of SLα/SLβ with carp TAC3 gene products, could induce a noticeable enhancement in SLα mRNA expression and these potentiating effects occurred with a parallel rise in NK3R transcript level after SLα/SLβ treatment. Interestingly, the stimulatory effects of SLα/SLβ on NK3R gene expression could be further potentiated by co-treatment with IGF-I/-II and simultaneous exposure of carp pituitary cells to SLα/SLβ and IGF-I/-II in the presence of TAC3 gene products was found to markedly elevated SLα mRNA expression (20 fold increase) and this synergistic stimulation was mediated by cAMP/PKA-, PLC/PKC- and Ca2+ -dependent cascades functionally coupled with NK3R activation. These findings suggest that local release of SLα via functional interactions with IGF-I/-II and TAC3/NK3R system may constitute a potent stimulatory signal for SLα gene expression in the carp pituitary via up-regulation of NK3R expression.

Highlights

  • Somatolactin (SL), the latest member of growth hormone (GH)/prolactin (PRL) family, is a fish-specific hormone released from the neurointermediate lobe (NIL) of the posterior pituitary[1]

  • The signal transduction mechanisms involved in SLαand SLβinduction of NK3R mRNA expression were elucidated and the functional role of NK3R expression and the post-receptor signaling pathways coupled with NK3R activation in the potentiating effects on SLαmRNA expression observed with cotreatment of insulin-like growth factors (IGFs)-I/-II and tachykinin 3 (TAC3) gene products was confirmed at the pituitary cell level

  • Given that (i) two somatolactin isoforms, SLαand SLβ, have been previously shown to trigger SLαsecretion and gene expression at the pituitary level[7], and (ii) TAC3a gene products could stimulate SLαsecretion and gene expression via activation of NK3R in carp pituitary cells[14], we examined the functional interaction between TAC3a gene products and SLs in their stimulatory activity on SLαgene expression

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Summary

Introduction

Somatolactin (SL), the latest member of growth hormone (GH)/prolactin (PRL) family, is a fish-specific hormone released from the neurointermediate lobe (NIL) of the posterior pituitary[1]. The investigation on SLαregulation by TAC3 gene products in the carp model have become more exciting with the recent demonstration that IGF-I/-II could act in a synergistic manner with TAC3 gene products, namely NKB and NKBRP, to up-regulate SLαgene expression at the pituitary level and this potentiating effect could be paralleled with the concurrent rise in NK3R expression induced by IGF-I/-II treatment. These new findings demonstrated for the first time that NK3R expression at the pituitary level could serve as a regulatory target for modulation of pituitary hormone gene expression in vertebrate species. Our studies for the first time provide evidence that local release of SLαand SLβcould interact with IGF-I/-II and TAC3 gene products to up-regulate SLαgene expression in the carp pituitary via stimulation of NK3R expression at the pituitary level

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