title: Leptin promotes the development of mouse preimplantation embryos in vitro.
abstract: Leptin acts as a modulator of diverse reproductive functions, and recent studies have implicated involvement of leptin in the early embryo development in mammal. The aim of this study was to investigate the expression of leptin and its receptor (OB-R) in mouse oocyte and preimplantation embryo, and to examine whether leptin influenced the early embryo development. Leptin mRNA was detected in blastocyst and hatched blastocyst, and two splice variants of OB-R (OB-Ra and OB-Rb) mRNAs were detected in oocytes, 1-cell, 2-cell, morula, blastocyst, and hatched blastocyst. As for the origin of leptin, both leptin mRNA and protein were identified in the oviduct epithelium and endometrium of pregnant mouse. In the pregnant mouse, the levels of leptin in uterine fluid were higher than those in nonpregnant mouse. Addition of leptin to embryo culture media promotes the development from 2-cell stage embryos to the blastocysts, fully expanded blastocysts and hatched blastocysts. This effect was neutralized by an antibody against the extracellular domain of OB-R. Leptin significantly increased the total cell number of blastocysts, and the effect was preferentially observed in the trophectoderm. These findings raise the possibility of a paracrine/autocrine leptin signaling system regulating the development of mouse preimplantation embryo.
authors.affiliation: Department of Obstetrics and Gynecology, Akita University School of Medicine, Hondo 1-1-1, Akita 010-8543, Japan. kawamurak@obgyn.med.akita-u.ac.jp
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Kawamura
authors.forename: Naoki
authors.initials: N
authors.lastname: Sato
authors.forename: Jun
authors.initials: J
authors.lastname: Fukuda
authors.forename: Hideya
authors.initials: H
authors.lastname: Kodama
authors.forename: Jin
authors.initials: J
authors.lastname: Kumagai
authors.forename: Hideo
authors.initials: H
authors.lastname: Tanikawa
authors.forename: Akira
authors.initials: A
authors.lastname: Nakamura
authors.forename: Toshinobu
authors.initials: T
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D019138:Antibodies, Blocking / Q000494:pharmacology; D001755:Blastocyst / Q000187:drug effects*; D002352:Carrier Proteins / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D002452:Cell Count; D002455:Cell Division / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D004717:Endometrium / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005187:Fallopian Tubes / Q000378:metabolism; D005260:Female; D005307:Fertilization in Vitro; D005455:Fluorescent Antibody Technique; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D020738:Leptin / Q000096:biosynthesis / Q000494:pharmacology*; D051379:Mice; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014599:Uterus / Q000378:metabolism
chemical_list: D019138:Antibodies, Blocking; D002352:Carrier Proteins; D020738:Leptin; D016376:Oligonucleotides, Antisense; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; C515447:leptin receptor, mouse