title: Maturation of bovine oocytes in the presence of leptin improves development and reduces apoptosis of in vitro-produced blastocysts.
abstract: The series of events associated with oocyte growth and maturation determines the oocyte's ability to undergo successful fertilization, cleavage and embryonic development. Among the molecules involved in these events, leptin has been identified as a modulator of oocyte function. Experiments were conducted to determine whether leptin treatment of oocytes during maturation affects their developmental capacity after fertilization and whether it has long-lasting effects on apoptosis and gene expression in the resulting blastocysts. Cumulus-oocyte complexes (COCs) were matured in serum-free medium containing 0 (control), 1, 10, or 100 ng/ml leptin or in medium supplemented with 10% (v/v) estrous cow serum (ECS). Addition of leptin during oocyte maturation had no effect on cleavage rate after fertilization. However, an increased proportion of oocytes that matured in the presence of 1 or 10 ng/ml leptin developed to blastocysts, which exhibited increased cell numbers. The proportion of apoptotic cells was reduced in blastocysts originating from leptin- or ECS-treated oocytes. Transcript levels of the genes encoding leptin receptor (LEPR), signal transducer and activator of transcription (STAT3), BCL2 associated X-protein (BAX), and baculoviral inhibitor of apoptosis protein repeat-containing 4 (BIRC4, also known as XIAP), were determined by reverse transcriptase-quantitative polymerase chain reaction analysis of expanded and hatched blastocysts. Depending on the dose used, leptin treatment of oocytes resulted in increased LEPR, STAT3, and BIRC4 mRNA levels and reduced BAX mRNA levels in blastocysts. In conclusion, leptin improved the ability of the oocyte to sustain embryonic development and had long-term effects on blastocyst apoptosis and transcript abundance of LEPR, STAT3, and apoptosis-associated genes.
authors.affiliation: Department of Molecular Animal Breeding and Biotechnology, Ludwig-Maximilian University, Oberschleissheim, Germany.
authors.forename: Marc
authors.initials: M
authors.lastname: Boelhauve
authors.forename: Fred
authors.initials: F
authors.lastname: Sinowatz
authors.forename: Eckhard
authors.initials: E
authors.lastname: Wolf
authors.forename: Fabíola F
authors.initials: FF
authors.lastname: Paula-Lopes
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000235:genetics; D001755:Blastocyst / Q000166:cytology* / Q000502:physiology; D002417:Cattle; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D047108:Embryonic Development; D005260:Female; D005307:Fertilization in Vitro / Q000379:methods*; D018507:Gene Expression Regulation, Developmental; D020738:Leptin / Q000378:metabolism / Q000494:pharmacology*; D009865:Oocytes / Q000187:drug effects / Q000502:physiology*; D011956:Receptors, Cell Surface / Q000235:genetics; D054411:Receptors, Leptin; D050796:STAT3 Transcription Factor / Q000235:genetics; D015398:Signal Transduction; D051636:X-Linked Inhibitor of Apoptosis Protein / Q000235:genetics; D051028:bcl-2-Associated X Protein / Q000235:genetics
chemical_list: C515448:LEPR protein, human; D020738:Leptin; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D050796:STAT3 Transcription Factor; D051636:X-Linked Inhibitor of Apoptosis Protein; C496866:XIAP protein, human; D051028:bcl-2-Associated X Protein