title: GnRH receptor signaling in tilapia pituitary cells: role of mitogen-activated protein kinase (MAPK).
abstract: The role of mitogen-activated protein kinase (MAPK, also known as extracellular signal regulated kinase; ERK) stimulation in gonadotropin-releasing hormone (GnRH) signaling was investigated in cultured pituitary cells of tilapia hybrids (Oreochromis niloticus x O. aureus). Exposure of the cells to salmon GnRH (sGnRH) resulted in a dose- and time-dependent elevation in ERK levels. The PKC activator, 1-O-tetradecanoyl phorbol-13-acetate (TPA) increased kinase levels, while addition of GnRH had no further effect. However, chronic exposure to TPA resulted in reduction of basal and GnRH-induced ERK elevation. When PKC was inhibited by GF109203X, the GnRH-elevated ERK levels were totally abolished. The role of MAPK activation on GPalpha, FSHbeta and LHbeta gene expression was determined by administration of MAPK-kinase (MEK) inhibitor (PD98059; PD). This inhibitor completely blocked GnRH-induced increases in ERK activity. Furthermore, it suppressed GPalpha and LHbeta mRNA responses to GnRH, but had no effect on FSHbeta transcript levels. PD also decreased basal LHbeta mRNA levels. These results indicate that in tilapia pituitary cells, GnRH activates MAPK cascade in a PKC-dependent manner. ERK is involved in GnRH elevation of GPalpha and LHbeta, but not in FSHbeta genes transcription.
authors.affiliation: Department of Zoology, Tel-Aviv University, 69978, Tel-Aviv, Israel. galgur@post.tau.ac.il
authors.forename: G
authors.initials: G
authors.lastname: Gur
authors.forename: D
authors.initials: D
authors.lastname: Bonfil
authors.forename: H
authors.initials: H
authors.lastname: Safarian
authors.forename: Z
authors.initials: Z
authors.lastname: Naor
authors.forename: Z
authors.initials: Z
authors.lastname: Yaron
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D004789:Enzyme Activation / Q000187:drug effects; D005640:Follicle Stimulating Hormone / Q000235:genetics; D037201:Follicle Stimulating Hormone, beta Subunit; D005786:Gene Expression Regulation / Q000187:drug effects; D015292:Glycoprotein Hormones, alpha Subunit / Q000235:genetics; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D006062:Gonadotropins / Q000235:genetics; D006824:Hybridization, Genetic; D007527:Isoenzymes / Q000037:antagonists & inhibitors / Q000378:metabolism; D007986:Luteinizing Hormone / Q000235:genetics; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism; D021122:Protein Subunits; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011966:Receptors, LHRH / Q000378:metabolism*; D012474:Salmon; D017210:Tilapia / Q000378:metabolism*; D013997:Time Factors
chemical_list: D037201:Follicle Stimulating Hormone, beta Subunit; D015292:Glycoprotein Hormones, alpha Subunit; D006062:Gonadotropins; D007527:Isoenzymes; D021122:Protein Subunits; D012333:RNA, Messenger; D011966:Receptors, LHRH; D007987:Gonadotropin-Releasing Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D011493:Protein Kinase C; D020928:Mitogen-Activated Protein Kinases