title: Nuclear oxysterol receptors, LXRs, are involved in the maintenance of mouse caput epididymidis structure and functions.
abstract: In this study we looked at the epididymides and spermatozoa of mice knocked-out for nuclear oxysterol receptors (LXR). We have shown that LXR-deficient mice exhibited upon ageing a severe disruption of their caput epididymides associated with abnormal accumulation of neutral lipids. The epididymis defaults were correlated with sperm head fragility and infertility. In agreement with the observed caput defect in transgenic animals in which both LXRalpha and LXRbeta isoforms were disrupted, we have shown here that both receptors are expressed in caput and cauda epididymides regions. LXRbeta was predominantly expressed throughout the mouse epididymis while the expression of LXRalpha was weaker. In addition, the expression of selected genes that can be considered as markers of adult epididymis function was monitored via Northern blots in the different single and double LXR-deficient backgrounds. Altogether, the data presented here suggest that LXR receptors are important actors in epididymis function.
authors.affiliation: Epididyme et Maturation des Gamètes, CNRS UMR 6547 GEEM, Université Blaise Pascal, 24, avenue des Landais, 63177 Aubière, France.
authors.forename: J-M
authors.initials: JM
authors.lastname: Frenoux
authors.forename: P
authors.initials: P
authors.lastname: Vernet
authors.forename: D H
authors.initials: DH
authors.lastname: Volle
authors.forename: A
authors.initials: A
authors.lastname: Britan
authors.forename: F
authors.initials: F
authors.lastname: Saez
authors.forename: A
authors.initials: A
authors.lastname: Kocer
authors.forename: J
authors.initials: J
authors.lastname: Henry-Berger
authors.forename: D J
authors.initials: DJ
authors.lastname: Mangelsdorf
authors.forename: J-M A
authors.initials: JM
authors.lastname: Lobaccaro
authors.forename: J R
authors.initials: JR
authors.lastname: Drevet
mesh_terms: D000818:Animals; D000924:Anticholesteremic Agents / Q000494:pharmacology; D004268:DNA-Binding Proteins; D004822:Epididymis / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D004847:Epithelial Cells / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000235:genetics; D006845:Hydrocarbons, Fluorinated; D000071518:Liver X Receptors; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D057093:Orphan Nuclear Receptors; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics* / Q000378:metabolism; D013075:Sperm Capacitation / Q000502:physiology*; D013094:Spermatozoa / Q000166:cytology / Q000502:physiology; D013449:Sulfonamides; D013735:Testicular Hormones / Q000235:genetics; D013739:Testosterone / Q000494:pharmacology; D014157:Transcription Factors / Q000235:genetics; D005466:Fluorocarbons; D000096926:Benzenesulfonamides
chemical_list: D000924:Anticholesteremic Agents; D004268:DNA-Binding Proteins; D005979:Glutathione Peroxidase; D006845:Hydrocarbons, Fluorinated; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors; D018160:Receptors, Cytoplasmic and Nuclear; D013449:Sulfonamides; D013735:Testicular Hormones; D013739:Testosterone; D014157:Transcription Factors; C000605214:Nr1h3 protein, mouse; C423915:T0901317; D005466:Fluorocarbons; D000096926:Benzenesulfonamides; C065788:transcription factor PEA3; C116888:Gpx3 protein, mouse; C080439:selenium-independent glutathione peroxidase