Prolactin inhibits cell loss and decreases matrix metalloproteinase expression in the involuting mouse mammary gland but fails to prevent cell loss in the mammary glands of mice expressing IGFBP-5 as a mammary transgene
Insulin-like growth factor-binding protein 5 (IGFBP-5) mediates involution of the mammary gland. The decrease in DNA content and mammary gland weight which accompanies involution was inhibited by prolactin (PRL) in wild-type but not transgenic mice expressing IGFBP-5. Phospho-STAT5 protein levels we...
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| Veröffentlicht in: | Journal of molecular endocrinology 2006-06, Vol.36 (3), p.435-448 |
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| creator | Flint, D J Boutinaud, M Whitelaw, C B A Allan, G J Kolb, A F |
| description | Insulin-like growth factor-binding protein 5 (IGFBP-5) mediates involution of the mammary gland. The decrease in DNA content and mammary gland weight which accompanies involution was inhibited by prolactin (PRL) in wild-type but not transgenic mice expressing IGFBP-5. Phospho-STAT5 protein levels were significantly lower in IGFBP-5 transgenic mice during lactation suggesting that IGFBP-5 antagonises PRL signalling in the mammary epithelium. In contrast, phospho-STAT3 levels increased during involution to a similar extent in both wild-type and transgenic mice and were unaffected by PRL. PRL inhibited gene expression of matrix metalloproteinases (MMPs) 3 and 12 but not tissue plasminogen activator or plasmin in wild-type and transgenic animals. The effects of PRL on MMPs appear to be indirect since PRL failed to inhibit MMP-3, -7 or -12 expression in HC-11 cells or in a co-transfection including an activated PRL receptor, STAT5 and a MMP-3-luciferase reporter gene. PRL is a potent inhibitor, both of cell death, an effect which is suppressed by IGFBP-5, and of MMP expression, which is independent of the actions of IGFBP-5. |
| doi_str_mv | 10.1677/jme.1.01873 |
| format | Article |
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The decrease in DNA content and mammary gland weight which accompanies involution was inhibited by prolactin (PRL) in wild-type but not transgenic mice expressing IGFBP-5. Phospho-STAT5 protein levels were significantly lower in IGFBP-5 transgenic mice during lactation suggesting that IGFBP-5 antagonises PRL signalling in the mammary epithelium. In contrast, phospho-STAT3 levels increased during involution to a similar extent in both wild-type and transgenic mice and were unaffected by PRL. PRL inhibited gene expression of matrix metalloproteinases (MMPs) 3 and 12 but not tissue plasminogen activator or plasmin in wild-type and transgenic animals. The effects of PRL on MMPs appear to be indirect since PRL failed to inhibit MMP-3, -7 or -12 expression in HC-11 cells or in a co-transfection including an activated PRL receptor, STAT5 and a MMP-3-luciferase reporter gene. PRL is a potent inhibitor, both of cell death, an effect which is suppressed by IGFBP-5, and of MMP expression, which is independent of the actions of IGFBP-5.</description><identifier>ISSN: 0952-5041</identifier><identifier>EISSN: 1479-6813</identifier><identifier>DOI: 10.1677/jme.1.01873</identifier><identifier>PMID: 16720715</identifier><language>eng</language><publisher>England: BioScientifica</publisher><subject>Animals ; Caseins - genetics ; Caseins - metabolism ; Cell Line ; Cricetinae ; Endocrinology and metabolism ; Female ; Fibrinolysin - metabolism ; Gene Expression Regulation, Enzymologic ; Genes, Reporter ; Human health and pathology ; Insulin-Like Growth Factor Binding Protein 5 - genetics ; Insulin-Like Growth Factor Binding Protein 5 - metabolism ; Lactation - physiology ; Life Sciences ; Mammary Glands, Animal - anatomy & histology ; Mammary Glands, Animal - physiology ; Matrix Metalloproteinases - genetics ; Matrix Metalloproteinases - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Prolactin - metabolism ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Receptors, Somatomedin - genetics ; Receptors, Somatomedin - metabolism ; Regular papers ; Signal Transduction - physiology ; Somatomedins - metabolism ; STAT3 Transcription Factor - genetics ; STAT3 Transcription Factor - metabolism ; STAT5 Transcription Factor - metabolism ; Tissue Plasminogen Activator - genetics ; Tissue Plasminogen Activator - metabolism ; Transgenes</subject><ispartof>Journal of molecular endocrinology, 2006-06, Vol.36 (3), p.435-448</ispartof><rights>2006 Society for Endocrinology</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b443t-528cf53727739dc24acf2d38913b2360b56755807d841cc00f8a156658ab74673</citedby><orcidid>0000-0003-0820-0966</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,3936,3937,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16720715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.inrae.fr/hal-02659039$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Flint, D J</creatorcontrib><creatorcontrib>Boutinaud, M</creatorcontrib><creatorcontrib>Whitelaw, C B A</creatorcontrib><creatorcontrib>Allan, G J</creatorcontrib><creatorcontrib>Kolb, A F</creatorcontrib><title>Prolactin inhibits cell loss and decreases matrix metalloproteinase expression in the involuting mouse mammary gland but fails to prevent cell loss in the mammary glands of mice expressing IGFBP-5 as a mammary transgene</title><title>Journal of molecular endocrinology</title><addtitle>J Mol Endocrinol</addtitle><description>Insulin-like growth factor-binding protein 5 (IGFBP-5) mediates involution of the mammary gland. The decrease in DNA content and mammary gland weight which accompanies involution was inhibited by prolactin (PRL) in wild-type but not transgenic mice expressing IGFBP-5. Phospho-STAT5 protein levels were significantly lower in IGFBP-5 transgenic mice during lactation suggesting that IGFBP-5 antagonises PRL signalling in the mammary epithelium. In contrast, phospho-STAT3 levels increased during involution to a similar extent in both wild-type and transgenic mice and were unaffected by PRL. PRL inhibited gene expression of matrix metalloproteinases (MMPs) 3 and 12 but not tissue plasminogen activator or plasmin in wild-type and transgenic animals. The effects of PRL on MMPs appear to be indirect since PRL failed to inhibit MMP-3, -7 or -12 expression in HC-11 cells or in a co-transfection including an activated PRL receptor, STAT5 and a MMP-3-luciferase reporter gene. PRL is a potent inhibitor, both of cell death, an effect which is suppressed by IGFBP-5, and of MMP expression, which is independent of the actions of IGFBP-5.</description><subject>Animals</subject><subject>Caseins - genetics</subject><subject>Caseins - metabolism</subject><subject>Cell Line</subject><subject>Cricetinae</subject><subject>Endocrinology and metabolism</subject><subject>Female</subject><subject>Fibrinolysin - metabolism</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Genes, Reporter</subject><subject>Human health and pathology</subject><subject>Insulin-Like Growth Factor Binding Protein 5 - genetics</subject><subject>Insulin-Like Growth Factor Binding Protein 5 - metabolism</subject><subject>Lactation - physiology</subject><subject>Life Sciences</subject><subject>Mammary Glands, Animal - anatomy & histology</subject><subject>Mammary Glands, Animal - physiology</subject><subject>Matrix Metalloproteinases - genetics</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred CBA</subject><subject>Mice, Transgenic</subject><subject>Prolactin - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Receptors, Somatomedin - genetics</subject><subject>Receptors, Somatomedin - metabolism</subject><subject>Regular papers</subject><subject>Signal Transduction - physiology</subject><subject>Somatomedins - metabolism</subject><subject>STAT3 Transcription Factor - genetics</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>STAT5 Transcription Factor - metabolism</subject><subject>Tissue Plasminogen Activator - genetics</subject><subject>Tissue Plasminogen Activator - metabolism</subject><subject>Transgenes</subject><issn>0952-5041</issn><issn>1479-6813</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1v1DAQhi0EokvhxB35hIRQFjuO4-TYVvRDWoke4Gw5zmTXlR0vtrOU38qfwWGjFpDgZMl-5pnxvAi9pmRNayE-3DlY0zWhjWBP0IpWoi3qhrKnaEVaXhacVPQEvYjxjhDKqaieo5NcVxJB-Qr9uA3eKp3MiM24M51JEWuwFlsfI1Zjj3vQAVSEiJ1KwdxjB0lZ6_fBJzBjfsFwvw8Qo_GzBKcd5OPg7ZStW-z8lBGnnFPhO97a2dlNCQ_K2IiTx7n2AGP6re0i-aMmYj9gZ_Rjt-y-ubo8vy04VnnUBzwFNcYtjPASPRuUjfBqOU_Rl8uPny-ui82nq5uLs03RVRVLBS8bPXAmSiFY2-uyUnooe9a0lHUlq0nHa8F5Q0TfVFRrQoZGUV7XvFGdqGrBTtG7o3enrNwHM08hvTLy-mwj5ztS1rwlrD3QzL49snl9XyeISToT55-rEfKiZN0QInjLMvj-COqQVxJgeDBTIufcZc5dUvkr90y_WbRT56B_ZJegM1AuM5rt7psJIDvjozZ58WYwWv3DSo9Ff7H_m-QnK_PODw</recordid><startdate>20060601</startdate><enddate>20060601</enddate><creator>Flint, D J</creator><creator>Boutinaud, M</creator><creator>Whitelaw, C B A</creator><creator>Allan, G J</creator><creator>Kolb, A F</creator><general>BioScientifica</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0003-0820-0966</orcidid></search><sort><creationdate>20060601</creationdate><title>Prolactin inhibits cell loss and decreases matrix metalloproteinase expression in the involuting mouse mammary gland but fails to prevent cell loss in the mammary glands of mice expressing IGFBP-5 as a mammary transgene</title><author>Flint, D J ; Boutinaud, M ; Whitelaw, C B A ; Allan, G J ; Kolb, A F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b443t-528cf53727739dc24acf2d38913b2360b56755807d841cc00f8a156658ab74673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Caseins - genetics</topic><topic>Caseins - metabolism</topic><topic>Cell Line</topic><topic>Cricetinae</topic><topic>Endocrinology and metabolism</topic><topic>Female</topic><topic>Fibrinolysin - metabolism</topic><topic>Gene Expression Regulation, Enzymologic</topic><topic>Genes, Reporter</topic><topic>Human health and pathology</topic><topic>Insulin-Like Growth Factor Binding Protein 5 - genetics</topic><topic>Insulin-Like Growth Factor Binding Protein 5 - metabolism</topic><topic>Lactation - physiology</topic><topic>Life Sciences</topic><topic>Mammary Glands, Animal - anatomy & histology</topic><topic>Mammary Glands, Animal - physiology</topic><topic>Matrix Metalloproteinases - genetics</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred CBA</topic><topic>Mice, Transgenic</topic><topic>Prolactin - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Receptors, Somatomedin - genetics</topic><topic>Receptors, Somatomedin - metabolism</topic><topic>Regular papers</topic><topic>Signal Transduction - physiology</topic><topic>Somatomedins - metabolism</topic><topic>STAT3 Transcription Factor - genetics</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>STAT5 Transcription Factor - metabolism</topic><topic>Tissue Plasminogen Activator - genetics</topic><topic>Tissue Plasminogen Activator - metabolism</topic><topic>Transgenes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Flint, D J</creatorcontrib><creatorcontrib>Boutinaud, M</creatorcontrib><creatorcontrib>Whitelaw, C B A</creatorcontrib><creatorcontrib>Allan, G J</creatorcontrib><creatorcontrib>Kolb, A F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Journal of molecular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Flint, D J</au><au>Boutinaud, M</au><au>Whitelaw, C B A</au><au>Allan, G J</au><au>Kolb, A F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prolactin inhibits cell loss and decreases matrix metalloproteinase expression in the involuting mouse mammary gland but fails to prevent cell loss in the mammary glands of mice expressing IGFBP-5 as a mammary transgene</atitle><jtitle>Journal of molecular endocrinology</jtitle><addtitle>J Mol Endocrinol</addtitle><date>2006-06-01</date><risdate>2006</risdate><volume>36</volume><issue>3</issue><spage>435</spage><epage>448</epage><pages>435-448</pages><issn>0952-5041</issn><eissn>1479-6813</eissn><abstract>Insulin-like growth factor-binding protein 5 (IGFBP-5) mediates involution of the mammary gland. The decrease in DNA content and mammary gland weight which accompanies involution was inhibited by prolactin (PRL) in wild-type but not transgenic mice expressing IGFBP-5. Phospho-STAT5 protein levels were significantly lower in IGFBP-5 transgenic mice during lactation suggesting that IGFBP-5 antagonises PRL signalling in the mammary epithelium. In contrast, phospho-STAT3 levels increased during involution to a similar extent in both wild-type and transgenic mice and were unaffected by PRL. PRL inhibited gene expression of matrix metalloproteinases (MMPs) 3 and 12 but not tissue plasminogen activator or plasmin in wild-type and transgenic animals. The effects of PRL on MMPs appear to be indirect since PRL failed to inhibit MMP-3, -7 or -12 expression in HC-11 cells or in a co-transfection including an activated PRL receptor, STAT5 and a MMP-3-luciferase reporter gene. PRL is a potent inhibitor, both of cell death, an effect which is suppressed by IGFBP-5, and of MMP expression, which is independent of the actions of IGFBP-5.</abstract><cop>England</cop><pub>BioScientifica</pub><pmid>16720715</pmid><doi>10.1677/jme.1.01873</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-0820-0966</orcidid><oa>free_for_read</oa></addata></record> |
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| issn | 0952-5041 1479-6813 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Society for Endocrinology Journals |
| subjects | Animals Caseins - genetics Caseins - metabolism Cell Line Cricetinae Endocrinology and metabolism Female Fibrinolysin - metabolism Gene Expression Regulation, Enzymologic Genes, Reporter Human health and pathology Insulin-Like Growth Factor Binding Protein 5 - genetics Insulin-Like Growth Factor Binding Protein 5 - metabolism Lactation - physiology Life Sciences Mammary Glands, Animal - anatomy & histology Mammary Glands, Animal - physiology Matrix Metalloproteinases - genetics Matrix Metalloproteinases - metabolism Mice Mice, Inbred C57BL Mice, Inbred CBA Mice, Transgenic Prolactin - metabolism Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Rats Receptors, Somatomedin - genetics Receptors, Somatomedin - metabolism Regular papers Signal Transduction - physiology Somatomedins - metabolism STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism STAT5 Transcription Factor - metabolism Tissue Plasminogen Activator - genetics Tissue Plasminogen Activator - metabolism Transgenes |
| title | Prolactin inhibits cell loss and decreases matrix metalloproteinase expression in the involuting mouse mammary gland but fails to prevent cell loss in the mammary glands of mice expressing IGFBP-5 as a mammary transgene |
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