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Am J Physiol Regul Integr Comp Physiol 289: R1634-R1643, 2005. First published July 7, 2005; doi:10.1152/ajpregu.00186.2005
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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

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

Christian Klausen,1 David L. Severson,2 John P. Chang,3 and Hamid R. Habibi1

1Departments of Biological Sciences and 2Pharmacology and Therapeutics, University of Calgary, Calgary, Alberta, Canada; and 3Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada

Submitted 15 March 2005 ; accepted in final form 24 June 2005

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-{alpha}, follicle-stimulating hormone (FSH)-{beta} and LH-{beta} 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-{alpha}-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.

pituitary; gene expression; goldfish; gonadotropes; neuroendocrinology; protein kinase C



Address for reprint requests and other correspondence: H. R. Habibi, Dept. of Biological Sciences, Univ. of Calgary, 2500 University Dr. N.W., Calgary, Alberta, Canada, T2N 1N4 (e-mail: habibi{at}ucalgary.ca)




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