Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs
Previously, we reported that administration of prolactin (PRL) during the early luteal phase in sows increases plasma progesterone concentrations. In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the ef...
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| Veröffentlicht in: | Journal of endocrinology 1998-11, Vol.159 (2), p.201-209 |
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| creator | Ciereszko, RE Petroff, BK Ottobre, AC Guan, Z Stokes, BT Ottobre, JS |
| description | Previously, we reported that administration of prolactin (PRL) during the early luteal phase in sows increases plasma progesterone concentrations. In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the effect of PRL and/or low-density lipoproteins (LDL) on progesterone production by porcine luteal cells derived from early corpora lutea, and (2) to assess the ability of PRL to activate phosphoinositide-specific phospholipase C (PI-PLC) and protein kinase C (PKC) in these luteal cells. Ovaries with early corpora lutea (day 1-2 of the oestrous cycle) were obtained from the slaughterhouse. Progesterone production by dispersed luteal cells was measured after treatment with PRL, phorbol 12-myristate 13-acetate or inhibitors of PKC in the presence or absence of LDL. LDL increased progesterone concentration in the incubation medium (304.5 vs 178.6 ng/ml in control, P |
| doi_str_mv | 10.1677/joe.0.1590201 |
| format | Article |
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In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the effect of PRL and/or low-density lipoproteins (LDL) on progesterone production by porcine luteal cells derived from early corpora lutea, and (2) to assess the ability of PRL to activate phosphoinositide-specific phospholipase C (PI-PLC) and protein kinase C (PKC) in these luteal cells. Ovaries with early corpora lutea (day 1-2 of the oestrous cycle) were obtained from the slaughterhouse. Progesterone production by dispersed luteal cells was measured after treatment with PRL, phorbol 12-myristate 13-acetate or inhibitors of PKC in the presence or absence of LDL. LDL increased progesterone concentration in the incubation medium (304.5 vs 178.6 ng/ml in control, P<0.05). PRL augmented LDL-stimulated progesterone secretion by luteal cells (to 416 ng/ml, P<0.05), but PRL alone did not affect progesterone production (209.6 ng/ml, P>0.05). Staurosporine, a PKC inhibitor, inhibited progesterone secretion stimulated by the combined action of LDL and PRL; however, such inhibition was not demonstrated when cells were treated with the PKC inhibitor, H-7. PKC activation was assessed by measuring the specific association of [H]phorbol dibutyrate (H-PDBu) with luteal cells after treatment with PRL or ionomycin (a positive control). PRL and ionomycin increased H-PDBu-specific binding in early luteal cells by 28+/-5.5% (within 5 min) and 70.2+/-19.3% (within 2 min) over control binding respectively (P<0.05). In addition, PRL did not augment the LDL-stimulated progesterone production in PKC-deficient cells. In contrast with PKC, total inositol phosphate accumulation, as well as intracellular free calcium concentrations, were not affected by PRL in the current study. We conclude that PRL, in the presence of LDL, stimulates progesterone production by early corpora lutea in vitro. Moreover, PRL appears to activate PKC, but not PI-PLC, in these cells. Thus intracellular transduction of the PRL signal may involve activation of PKC that is not dependent on PI-PLC.</description><identifier>ISSN: 0022-0795</identifier><identifier>EISSN: 1479-6805</identifier><identifier>DOI: 10.1677/joe.0.1590201</identifier><identifier>PMID: 9795359</identifier><identifier>CODEN: JOENAK</identifier><language>eng</language><publisher>Colchester: BioScientifica</publisher><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology ; Animals ; Biological and medical sciences ; Carcinogens - pharmacology ; Cells, Cultured ; Corpus Luteum - drug effects ; Corpus Luteum - metabolism ; Drug Synergism ; Enzyme Activation ; Enzyme Inhibitors - pharmacology ; Female ; Fundamental and applied biological sciences. Psychology ; Hormone metabolism and regulation ; Ionomycin - pharmacology ; Ionophores - pharmacology ; Lipoproteins, LDL - pharmacology ; Luteal Phase - metabolism ; Mammalian female genital system ; Phorbol 12,13-Dibutyrate - metabolism ; Progesterone - biosynthesis ; Progesterone - blood ; Prolactin - pharmacology ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - metabolism ; Staurosporine - pharmacology ; Stimulation, Chemical ; Swine - metabolism ; Tetradecanoylphorbol Acetate - pharmacology ; Type C Phospholipases - metabolism ; Vertebrates: reproduction</subject><ispartof>Journal of endocrinology, 1998-11, Vol.159 (2), p.201-209</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b511t-5ccf036bdb2df4e5dcde6827fe118e444dd8d3ef00faddd584ae8a83f8ee81533</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1619383$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9795359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ciereszko, RE</creatorcontrib><creatorcontrib>Petroff, BK</creatorcontrib><creatorcontrib>Ottobre, AC</creatorcontrib><creatorcontrib>Guan, Z</creatorcontrib><creatorcontrib>Stokes, BT</creatorcontrib><creatorcontrib>Ottobre, JS</creatorcontrib><title>Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs</title><title>Journal of endocrinology</title><addtitle>J Endocrinol</addtitle><description>Previously, we reported that administration of prolactin (PRL) during the early luteal phase in sows increases plasma progesterone concentrations. In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the effect of PRL and/or low-density lipoproteins (LDL) on progesterone production by porcine luteal cells derived from early corpora lutea, and (2) to assess the ability of PRL to activate phosphoinositide-specific phospholipase C (PI-PLC) and protein kinase C (PKC) in these luteal cells. Ovaries with early corpora lutea (day 1-2 of the oestrous cycle) were obtained from the slaughterhouse. Progesterone production by dispersed luteal cells was measured after treatment with PRL, phorbol 12-myristate 13-acetate or inhibitors of PKC in the presence or absence of LDL. LDL increased progesterone concentration in the incubation medium (304.5 vs 178.6 ng/ml in control, P<0.05). PRL augmented LDL-stimulated progesterone secretion by luteal cells (to 416 ng/ml, P<0.05), but PRL alone did not affect progesterone production (209.6 ng/ml, P>0.05). Staurosporine, a PKC inhibitor, inhibited progesterone secretion stimulated by the combined action of LDL and PRL; however, such inhibition was not demonstrated when cells were treated with the PKC inhibitor, H-7. PKC activation was assessed by measuring the specific association of [H]phorbol dibutyrate (H-PDBu) with luteal cells after treatment with PRL or ionomycin (a positive control). PRL and ionomycin increased H-PDBu-specific binding in early luteal cells by 28+/-5.5% (within 5 min) and 70.2+/-19.3% (within 2 min) over control binding respectively (P<0.05). In addition, PRL did not augment the LDL-stimulated progesterone production in PKC-deficient cells. In contrast with PKC, total inositol phosphate accumulation, as well as intracellular free calcium concentrations, were not affected by PRL in the current study. We conclude that PRL, in the presence of LDL, stimulates progesterone production by early corpora lutea in vitro. Moreover, PRL appears to activate PKC, but not PI-PLC, in these cells. Thus intracellular transduction of the PRL signal may involve activation of PKC that is not dependent on PI-PLC.</description><subject>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Carcinogens - pharmacology</subject><subject>Cells, Cultured</subject><subject>Corpus Luteum - drug effects</subject><subject>Corpus Luteum - metabolism</subject><subject>Drug Synergism</subject><subject>Enzyme Activation</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hormone metabolism and regulation</subject><subject>Ionomycin - pharmacology</subject><subject>Ionophores - pharmacology</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Luteal Phase - metabolism</subject><subject>Mammalian female genital system</subject><subject>Phorbol 12,13-Dibutyrate - metabolism</subject><subject>Progesterone - biosynthesis</subject><subject>Progesterone - blood</subject><subject>Prolactin - pharmacology</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - metabolism</subject><subject>Staurosporine - pharmacology</subject><subject>Stimulation, Chemical</subject><subject>Swine - metabolism</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Type C Phospholipases - metabolism</subject><subject>Vertebrates: reproduction</subject><issn>0022-0795</issn><issn>1479-6805</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtLxDAQxoMouj6OHoUcvFaTpmnTo4gvWPCi55Imk22kbUqmi-x_b0sXBUFP8_rNN8NHyCVnNzwvituPADdTKkuWMn5AVjwryiRXTB6SFWNpmrCilCfkFPGDMS55IY7JcTn1hCxXZLhDBMQO-pEGR8cGaAem0b3HjtY7-tl409Ahhlab0fcUR99tWz0Czs0N4Agx9DAXdjsRoZ-3QMd2R02IQ4iattsR9Kw--A2ekyOnW4SLfTwj748Pb_fPyfr16eX-bp3UkvMxkcY4JvLa1ql1GUhrLOQqLRxwriDLMmuVFeAYc9paK1WmQWklnAJQXApxRpJF18SAGMFVQ_SdjruKs2o2rpqMq6Z0MW7irxZ-2NYd2G9679Q0v97PNRrduqh74_FHNOelUPPZbMEav2k-fYSq9gGNn_z1zhv953WxrP2i___5C5qknJg</recordid><startdate>19981101</startdate><enddate>19981101</enddate><creator>Ciereszko, RE</creator><creator>Petroff, BK</creator><creator>Ottobre, AC</creator><creator>Guan, Z</creator><creator>Stokes, BT</creator><creator>Ottobre, JS</creator><general>BioScientifica</general><general>Portland Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19981101</creationdate><title>Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs</title><author>Ciereszko, RE ; Petroff, BK ; Ottobre, AC ; Guan, Z ; Stokes, BT ; Ottobre, JS</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b511t-5ccf036bdb2df4e5dcde6827fe118e444dd8d3ef00faddd584ae8a83f8ee81533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Carcinogens - pharmacology</topic><topic>Cells, Cultured</topic><topic>Corpus Luteum - drug effects</topic><topic>Corpus Luteum - metabolism</topic><topic>Drug Synergism</topic><topic>Enzyme Activation</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hormone metabolism and regulation</topic><topic>Ionomycin - pharmacology</topic><topic>Ionophores - pharmacology</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Luteal Phase - metabolism</topic><topic>Mammalian female genital system</topic><topic>Phorbol 12,13-Dibutyrate - metabolism</topic><topic>Progesterone - biosynthesis</topic><topic>Progesterone - blood</topic><topic>Prolactin - pharmacology</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - metabolism</topic><topic>Staurosporine - pharmacology</topic><topic>Stimulation, Chemical</topic><topic>Swine - metabolism</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Type C Phospholipases - metabolism</topic><topic>Vertebrates: reproduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ciereszko, RE</creatorcontrib><creatorcontrib>Petroff, BK</creatorcontrib><creatorcontrib>Ottobre, AC</creatorcontrib><creatorcontrib>Guan, Z</creatorcontrib><creatorcontrib>Stokes, BT</creatorcontrib><creatorcontrib>Ottobre, JS</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Journal of endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ciereszko, RE</au><au>Petroff, BK</au><au>Ottobre, AC</au><au>Guan, Z</au><au>Stokes, BT</au><au>Ottobre, JS</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs</atitle><jtitle>Journal of endocrinology</jtitle><addtitle>J Endocrinol</addtitle><date>1998-11-01</date><risdate>1998</risdate><volume>159</volume><issue>2</issue><spage>201</spage><epage>209</epage><pages>201-209</pages><issn>0022-0795</issn><eissn>1479-6805</eissn><coden>JOENAK</coden><abstract>Previously, we reported that administration of prolactin (PRL) during the early luteal phase in sows increases plasma progesterone concentrations. In the current study, we searched for the mechanisms by which PRL exerts this luteotrophic effect. The objectives of the study were (1) to examine the effect of PRL and/or low-density lipoproteins (LDL) on progesterone production by porcine luteal cells derived from early corpora lutea, and (2) to assess the ability of PRL to activate phosphoinositide-specific phospholipase C (PI-PLC) and protein kinase C (PKC) in these luteal cells. Ovaries with early corpora lutea (day 1-2 of the oestrous cycle) were obtained from the slaughterhouse. Progesterone production by dispersed luteal cells was measured after treatment with PRL, phorbol 12-myristate 13-acetate or inhibitors of PKC in the presence or absence of LDL. LDL increased progesterone concentration in the incubation medium (304.5 vs 178.6 ng/ml in control, P<0.05). PRL augmented LDL-stimulated progesterone secretion by luteal cells (to 416 ng/ml, P<0.05), but PRL alone did not affect progesterone production (209.6 ng/ml, P>0.05). Staurosporine, a PKC inhibitor, inhibited progesterone secretion stimulated by the combined action of LDL and PRL; however, such inhibition was not demonstrated when cells were treated with the PKC inhibitor, H-7. PKC activation was assessed by measuring the specific association of [H]phorbol dibutyrate (H-PDBu) with luteal cells after treatment with PRL or ionomycin (a positive control). PRL and ionomycin increased H-PDBu-specific binding in early luteal cells by 28+/-5.5% (within 5 min) and 70.2+/-19.3% (within 2 min) over control binding respectively (P<0.05). In addition, PRL did not augment the LDL-stimulated progesterone production in PKC-deficient cells. In contrast with PKC, total inositol phosphate accumulation, as well as intracellular free calcium concentrations, were not affected by PRL in the current study. We conclude that PRL, in the presence of LDL, stimulates progesterone production by early corpora lutea in vitro. Moreover, PRL appears to activate PKC, but not PI-PLC, in these cells. Thus intracellular transduction of the PRL signal may involve activation of PKC that is not dependent on PI-PLC.</abstract><cop>Colchester</cop><pub>BioScientifica</pub><pmid>9795359</pmid><doi>10.1677/joe.0.1590201</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - pharmacology Animals Biological and medical sciences Carcinogens - pharmacology Cells, Cultured Corpus Luteum - drug effects Corpus Luteum - metabolism Drug Synergism Enzyme Activation Enzyme Inhibitors - pharmacology Female Fundamental and applied biological sciences. Psychology Hormone metabolism and regulation Ionomycin - pharmacology Ionophores - pharmacology Lipoproteins, LDL - pharmacology Luteal Phase - metabolism Mammalian female genital system Phorbol 12,13-Dibutyrate - metabolism Progesterone - biosynthesis Progesterone - blood Prolactin - pharmacology Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Staurosporine - pharmacology Stimulation, Chemical Swine - metabolism Tetradecanoylphorbol Acetate - pharmacology Type C Phospholipases - metabolism Vertebrates: reproduction |
| title | Assessment of the mechanism by which prolactin stimulates progesterone production by early corpora lutea of pigs |
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