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REPRODUCTION-DEVELOPMENT |
Department of Obstetrics and Gynecology (K.K., N.S., J.F., J.K., H.T., T.T.), Department of Medical Information Science (A.N.), Akita University School of Medicine, and Akita University College of Allied Medical Science (H.K.), Akita 010-0041, Japan
Address all correspondence and requests for reprints to: Kazuhiro Kawamura, Department of Obstetrics and Gynecology, Akita University School of Medicine, Hondo 1-1-1, Akita 010-8543, Japan. E-mail: . kawamurak{at}obgyn.med.akita-u.ac.jp
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.
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