Grass carp prolactin: Molecular cloning, tissue expression, intrapituitary autoregulation by prolactin and paracrine regulation by growth hormone and luteinizing hormone

• Cloning of grass carp PRL and confirmation of its pituitary and gonadal expression.
• PRL reduced PRL secretion but elevated PRL gene expression in carp pituitary cells.
• GH induced but LH suppressed PRL release and gene expression at pituitary cell level.
• These PRL responses might involve changes in PRL mRNA stability/gene transcription.

Prolactin (PRL), a pituitary hormone with diverse functions, is well-documented to be under the control of both hypothalamic and peripheral signals. Intrapituitary modulation of PRL expression via autocrine/paracrine mechanisms has also been reported, but similar information is still lacking in lower vertebrates. To shed light on autocrine/paracrine regulation of PRL in fish model, grass carp PRL was cloned and its expression in the carp pituitary has been confirmed. In grass carp pituitary cells, local secretion of PRL could suppress PRL release with concurrent rises in PRL production and mRNA levels. Paracrine stimulation by growth hormone (GH) was found to up- regulate PRL secretion, PRL production and PRL transcript expression, whereas the opposite was true for the local actions of luteinizing hormone (LH). Apparently, local interactions of PRL, GH and LH via autocrine/paracrine mechanisms could modify PRL production in carp pituitary cells through differential regulation of PRL mRNA stability and gene transcription.

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