Absence of Nuclear Receptors for Oxysterols Liver X Receptor Induces Ovarian Hyperstimulation Syndrome in Mice
Ovarian hyperstimulation syndrome is a frequent complication occurring during in vitro fertilization cycles. It is characterized by a massive ovarian enlargement associated with an accumulation of extra vascular fluid. Here we show that liver X receptor (LXR)-α and LXR-β deficient mice present many...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2009-07, Vol.150 (7), p.3369-3375 |
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| creator | Mouzat, Kevin Volat, Fanny Baron, Silvère Alves, Georges Pommier, Aurélien J. C Volle, David H Marceau, Geoffroy DeHaze, Angélique Déchelotte, Pierre Duggavathi, Raj Caira, Françoise Lobaccaro, Jean-Marc A |
| description | Ovarian hyperstimulation syndrome is a frequent complication occurring during in vitro fertilization cycles. It is characterized by a massive ovarian enlargement associated with an accumulation of extra vascular fluid. Here we show that liver X receptor (LXR)-α and LXR-β deficient mice present many clinical and biological signs of ovarian hyperstimulation syndrome: ovarian enlargement, hemorrhagic corpora lutea, increased ovarian vascular permeability, and elevated estradiol. Ovulation stimulation resulted in excessive ovarian response to exogenous gonadotropins because follicle number and estradiol production were higher in transgenic mice. LXR deficiency also leads to perturbations in general inflammatory status, associated with ovarian il-6 deregulation. Upon treatment with the synthetic LXR agonist T09101317, serum estradiol and expression of star and cyp11a1 genes were markedly increased in wild-type mice, showing that LXRs are key regulators of ovarian steroidogenesis. These results suggest that LXRs control the ovulation by regulating endocrine and vascular processes.
Female mice lacking nuclear receptors for oxysterols LXR develop many biological and clinical signs of ovarian hyperstimulation syndrome when undergoing an ovulation induction treatment. |
| doi_str_mv | 10.1210/en.2008-1519 |
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Female mice lacking nuclear receptors for oxysterols LXR develop many biological and clinical signs of ovarian hyperstimulation syndrome when undergoing an ovulation induction treatment.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2008-1519</identifier><identifier>PMID: 19325005</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>17β-Estradiol ; Animals ; Biological and medical sciences ; Chorionic Gonadotropin - pharmacology ; Deregulation ; DNA-Binding Proteins - deficiency ; DNA-Binding Proteins - physiology ; Enlargement ; Estradiol - biosynthesis ; Female ; Fundamental and applied biological sciences. Psychology ; Gonadotropins ; Hydrocarbons, Fluorinated - pharmacology ; In vitro fertilization ; Inflammation - physiopathology ; Liver ; Liver X Receptors ; Mice ; Mice, Knockout ; Nuclear receptors ; Orphan Nuclear Receptors ; Ovarian hyperstimulation syndrome ; Ovarian Hyperstimulation Syndrome - etiology ; Ovarian Hyperstimulation Syndrome - pathology ; Ovulation ; Ovulation Induction ; Pituitary (anterior) ; Receptors ; Receptors, Cytoplasmic and Nuclear - deficiency ; Receptors, Cytoplasmic and Nuclear - physiology ; Sex hormones ; Steroidogenesis ; Sulfonamides - pharmacology ; Transgenic mice ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2009-07, Vol.150 (7), p.3369-3375</ispartof><rights>Copyright © 2009 by The Endocrine Society 2009</rights><rights>2009 INIST-CNRS</rights><rights>Copyright © 2009 by The Endocrine Society</rights><rights>Copyright © 2009 by The Endocrine Society 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c516t-4c19f9362ab99df7170b395dca663a09b93e06331256aba240b0f80f194e60873</citedby><cites>FETCH-LOGICAL-c516t-4c19f9362ab99df7170b395dca663a09b93e06331256aba240b0f80f194e60873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21709560$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19325005$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mouzat, Kevin</creatorcontrib><creatorcontrib>Volat, Fanny</creatorcontrib><creatorcontrib>Baron, Silvère</creatorcontrib><creatorcontrib>Alves, Georges</creatorcontrib><creatorcontrib>Pommier, Aurélien J. C</creatorcontrib><creatorcontrib>Volle, David H</creatorcontrib><creatorcontrib>Marceau, Geoffroy</creatorcontrib><creatorcontrib>DeHaze, Angélique</creatorcontrib><creatorcontrib>Déchelotte, Pierre</creatorcontrib><creatorcontrib>Duggavathi, Raj</creatorcontrib><creatorcontrib>Caira, Françoise</creatorcontrib><creatorcontrib>Lobaccaro, Jean-Marc A</creatorcontrib><title>Absence of Nuclear Receptors for Oxysterols Liver X Receptor Induces Ovarian Hyperstimulation Syndrome in Mice</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Ovarian hyperstimulation syndrome is a frequent complication occurring during in vitro fertilization cycles. It is characterized by a massive ovarian enlargement associated with an accumulation of extra vascular fluid. Here we show that liver X receptor (LXR)-α and LXR-β deficient mice present many clinical and biological signs of ovarian hyperstimulation syndrome: ovarian enlargement, hemorrhagic corpora lutea, increased ovarian vascular permeability, and elevated estradiol. Ovulation stimulation resulted in excessive ovarian response to exogenous gonadotropins because follicle number and estradiol production were higher in transgenic mice. LXR deficiency also leads to perturbations in general inflammatory status, associated with ovarian il-6 deregulation. Upon treatment with the synthetic LXR agonist T09101317, serum estradiol and expression of star and cyp11a1 genes were markedly increased in wild-type mice, showing that LXRs are key regulators of ovarian steroidogenesis. These results suggest that LXRs control the ovulation by regulating endocrine and vascular processes.
Female mice lacking nuclear receptors for oxysterols LXR develop many biological and clinical signs of ovarian hyperstimulation syndrome when undergoing an ovulation induction treatment.</description><subject>17β-Estradiol</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chorionic Gonadotropin - pharmacology</subject><subject>Deregulation</subject><subject>DNA-Binding Proteins - deficiency</subject><subject>DNA-Binding Proteins - physiology</subject><subject>Enlargement</subject><subject>Estradiol - biosynthesis</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gonadotropins</subject><subject>Hydrocarbons, Fluorinated - pharmacology</subject><subject>In vitro fertilization</subject><subject>Inflammation - physiopathology</subject><subject>Liver</subject><subject>Liver X Receptors</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Nuclear receptors</subject><subject>Orphan Nuclear Receptors</subject><subject>Ovarian hyperstimulation syndrome</subject><subject>Ovarian Hyperstimulation Syndrome - etiology</subject><subject>Ovarian Hyperstimulation Syndrome - pathology</subject><subject>Ovulation</subject><subject>Ovulation Induction</subject><subject>Pituitary (anterior)</subject><subject>Receptors</subject><subject>Receptors, Cytoplasmic and Nuclear - deficiency</subject><subject>Receptors, Cytoplasmic and Nuclear - physiology</subject><subject>Sex hormones</subject><subject>Steroidogenesis</subject><subject>Sulfonamides - pharmacology</subject><subject>Transgenic mice</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc2L1DAYxoMo7rh68ywBUS92zXcnF2FZdt2F0QE_wFtI07eapU1q0g7Of2_LlFkVPYWQH89HHoSeUnJGGSVvIJwxQtYFlVTfQyuqhSxKWpL7aEUI5UXJWHmCHuV8O12FEPwhOqGaM0mIXKFwXmUIDnBs8IfRtWAT_ggO-iGmjJuY8PbnPg-QYpvxxu8g4a9HAN-EenSQ8XZnk7cBX-97SHnw3djawceAP-1DnWIH2Af83jt4jB40ts3wZDlP0Zery88X18Vm--7m4nxTOEnVUAhHdaO5YrbSum7mOhXXsnZWKW6JrjQHojinTCpbWSZIRZo1aabyoMi65Kfo7UG3H6sOagdhSLY1ffKdTXsTrTd_vgT_3XyLO8NKwiVlk8DLRSDFHyPkwXQ-O2hbGyCO2ahSUCrV7PT8L_A2jilM5QynnEgtRDnLvT5QLsWcEzTHKJSYeUYDwcwzmnnGCX_2e_w7eNltAl4sgM3Otk2ywfl85Nj0YVoqMnGvDlwc-_9ZFoslP5AQ6uiSD9AnyPmuzT-D_gIIMsLj</recordid><startdate>20090701</startdate><enddate>20090701</enddate><creator>Mouzat, Kevin</creator><creator>Volat, Fanny</creator><creator>Baron, Silvère</creator><creator>Alves, Georges</creator><creator>Pommier, Aurélien J. C</creator><creator>Volle, David H</creator><creator>Marceau, Geoffroy</creator><creator>DeHaze, Angélique</creator><creator>Déchelotte, Pierre</creator><creator>Duggavathi, Raj</creator><creator>Caira, Françoise</creator><creator>Lobaccaro, Jean-Marc A</creator><general>Endocrine Society</general><general>Oxford University Press</general><general>The Endocrine Society</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><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090701</creationdate><title>Absence of Nuclear Receptors for Oxysterols Liver X Receptor Induces Ovarian Hyperstimulation Syndrome in Mice</title><author>Mouzat, Kevin ; Volat, Fanny ; Baron, Silvère ; Alves, Georges ; Pommier, Aurélien J. C ; Volle, David H ; Marceau, Geoffroy ; DeHaze, Angélique ; Déchelotte, Pierre ; Duggavathi, Raj ; Caira, Françoise ; Lobaccaro, Jean-Marc A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c516t-4c19f9362ab99df7170b395dca663a09b93e06331256aba240b0f80f194e60873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>17β-Estradiol</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Chorionic Gonadotropin - pharmacology</topic><topic>Deregulation</topic><topic>DNA-Binding Proteins - deficiency</topic><topic>DNA-Binding Proteins - physiology</topic><topic>Enlargement</topic><topic>Estradiol - biosynthesis</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gonadotropins</topic><topic>Hydrocarbons, Fluorinated - pharmacology</topic><topic>In vitro fertilization</topic><topic>Inflammation - physiopathology</topic><topic>Liver</topic><topic>Liver X Receptors</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Nuclear receptors</topic><topic>Orphan Nuclear Receptors</topic><topic>Ovarian hyperstimulation syndrome</topic><topic>Ovarian Hyperstimulation Syndrome - etiology</topic><topic>Ovarian Hyperstimulation Syndrome - pathology</topic><topic>Ovulation</topic><topic>Ovulation Induction</topic><topic>Pituitary (anterior)</topic><topic>Receptors</topic><topic>Receptors, Cytoplasmic and Nuclear - deficiency</topic><topic>Receptors, Cytoplasmic and Nuclear - physiology</topic><topic>Sex hormones</topic><topic>Steroidogenesis</topic><topic>Sulfonamides - pharmacology</topic><topic>Transgenic mice</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mouzat, Kevin</creatorcontrib><creatorcontrib>Volat, Fanny</creatorcontrib><creatorcontrib>Baron, Silvère</creatorcontrib><creatorcontrib>Alves, Georges</creatorcontrib><creatorcontrib>Pommier, Aurélien J. 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C</au><au>Volle, David H</au><au>Marceau, Geoffroy</au><au>DeHaze, Angélique</au><au>Déchelotte, Pierre</au><au>Duggavathi, Raj</au><au>Caira, Françoise</au><au>Lobaccaro, Jean-Marc A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absence of Nuclear Receptors for Oxysterols Liver X Receptor Induces Ovarian Hyperstimulation Syndrome in Mice</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2009-07-01</date><risdate>2009</risdate><volume>150</volume><issue>7</issue><spage>3369</spage><epage>3375</epage><pages>3369-3375</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Ovarian hyperstimulation syndrome is a frequent complication occurring during in vitro fertilization cycles. It is characterized by a massive ovarian enlargement associated with an accumulation of extra vascular fluid. Here we show that liver X receptor (LXR)-α and LXR-β deficient mice present many clinical and biological signs of ovarian hyperstimulation syndrome: ovarian enlargement, hemorrhagic corpora lutea, increased ovarian vascular permeability, and elevated estradiol. Ovulation stimulation resulted in excessive ovarian response to exogenous gonadotropins because follicle number and estradiol production were higher in transgenic mice. LXR deficiency also leads to perturbations in general inflammatory status, associated with ovarian il-6 deregulation. Upon treatment with the synthetic LXR agonist T09101317, serum estradiol and expression of star and cyp11a1 genes were markedly increased in wild-type mice, showing that LXRs are key regulators of ovarian steroidogenesis. These results suggest that LXRs control the ovulation by regulating endocrine and vascular processes.
Female mice lacking nuclear receptors for oxysterols LXR develop many biological and clinical signs of ovarian hyperstimulation syndrome when undergoing an ovulation induction treatment.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>19325005</pmid><doi>10.1210/en.2008-1519</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 17β-Estradiol Animals Biological and medical sciences Chorionic Gonadotropin - pharmacology Deregulation DNA-Binding Proteins - deficiency DNA-Binding Proteins - physiology Enlargement Estradiol - biosynthesis Female Fundamental and applied biological sciences. Psychology Gonadotropins Hydrocarbons, Fluorinated - pharmacology In vitro fertilization Inflammation - physiopathology Liver Liver X Receptors Mice Mice, Knockout Nuclear receptors Orphan Nuclear Receptors Ovarian hyperstimulation syndrome Ovarian Hyperstimulation Syndrome - etiology Ovarian Hyperstimulation Syndrome - pathology Ovulation Ovulation Induction Pituitary (anterior) Receptors Receptors, Cytoplasmic and Nuclear - deficiency Receptors, Cytoplasmic and Nuclear - physiology Sex hormones Steroidogenesis Sulfonamides - pharmacology Transgenic mice Vertebrates: endocrinology |
| title | Absence of Nuclear Receptors for Oxysterols Liver X Receptor Induces Ovarian Hyperstimulation Syndrome in Mice |
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