title: Altered expression of Armet and Mrlp51 in the oocyte, preimplantation embryo, and brain of mice following oocyte in vitro maturation but postnatal brain development and cognitive function are normal.
abstract: Despite the efforts to recapitulate the follicle environment, oocytes from in vitro maturation (IVM) have poorer developmental potential than those matured in vivo and the effects on the resultant offspring are of concern. The aim of this study was to determine altered gene expression in oocytes following IVM and to evaluate the expression of the arginine rich, mutated in early stage of tumors gene (Armet) and mitochondrial ribosomal protein L51 (Mrpl51) in embryos and brains of fetal/postnatal mice and the brain development of IVM offspring. An IVM mouse model was established while oocytes matured in vivo were used as the controls. Suppressive subtractive hybridization (SSH) and RT-PCR/western blot were used to analyze the differential expression of genes/proteins between IVM and the control group. HE staining and water maze were used to assess the histological changes in brain tissue and cognition of the offspring. The rates of fertilization, cleavage, and live birth were significantly decreased in IVM group. Thirteen genes were upregulated in IVM oocytes compared with the control, including Armet and Mrpl51. The higher level of Armet in IVM oocytes was retained in brain of newborn mice, which could be related to the upregulation of activating transcription factor 6 (Atf6) and X-box binding protein 1 (Xbp1), while Mrpl51 was expressed normally in brain of postnatal mice. No significant differences were detected in brain weight, neuronal counts, and the cognition in the offspring between the two groups. The present results suggested that IVM could affect the pregnancy outcome and the Armet and Mrpl51 gene/protein expression. The change in Armet expression lasted while the change of Mrpl51 disappeared after birth. However, the brain development of the offspring seemed to be unaffected by IVM.
authors: Department of Reproductive Endocrinology, Key Laboratory of Reproductive Genetics, Ministry of Education, Women's Hospital, Zhejiang University School of Medicine, 1 Xueshi Road, Hangzhou 310006, China.
authors: Ning
authors: N
authors: Wang
authors: Liya
authors: L
authors: Wang
authors: Fang
authors: F
authors: Le
authors: Qitao
authors: Q
authors: Zhan
authors: Yingming
authors: Y
authors: Zheng
authors: Guolian
authors: G
authors: Ding
authors: Xijing
authors: X
authors: Chen
authors: Jianzhong
authors: J
authors: Sheng
authors: Minyue
authors: M
authors: Dong
authors: Hefeng
authors: H
authors: Huang
authors: Fan
authors: F
authors: Jin
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001755:Blastocyst / Q000378:metabolism*; D001921:Brain / Q000254:growth & development* / Q000378:metabolism* / Q000502:physiology; D002478:Cells, Cultured; D003071:Cognition / Q000502:physiology*; D046149:Embryo Culture Techniques; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D009414:Nerve Growth Factors / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D009865:Oocytes / Q000378:metabolism*; D009866:Oogenesis / Q000235:genetics / Q000502:physiology; D036801:Parturition / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D011247:Pregnancy; D012269:Ribosomal Proteins / Q000235:genetics* / Q000378:metabolism / Q000502:physiology
chemical_list: C534671:MANF protein, mouse; D024101:Mitochondrial Proteins; D009414:Nerve Growth Factors; D012269:Ribosomal Proteins; C568599:mitochondrial ribosomal protein L51, mouse