title: No loss of genomic imprinting of IGF-II and H19 in placentas of diabetic pregnancies with fetal macrosomia.
abstract: OBJECTIVE
  Fetal macrosomia is a common complication of maternal diabetes mellitus and is associated with substantial morbidity, but the precise cellular and molecular mechanisms that induce fetal macrosomia are not well understood. The imprinted genes IGF-II and H19 are crucial for placental development and fetal growth. The term placentas from diabetic pregnancies express more insulin-like growth factor II (IGF-II) than those from normal pregnancies. Deregulation of their imprinting status is observed in the macrosomia-associated syndrome, the Beckwith-Wiedemann syndrome. The aim of this study was to determine whether loss of imprinting hence biallelic expression was also a hallmark of macrosomia in diabetic pregnancies.
  
  
  METHODS
  IGF-II and H19 maternal and paternal expressions were studied in placentas from two groups of type 1 diabetic mothers: one with macrosomic babies and the other with babies of normal weight. Maternal or paternal allele specific expressions were defined by using DNA polymorphic markers of the IGF-II and H19 genes. RFLP analysis was performed on PCR products from genomic DNA of the father, the mother and the child, and on RT-PCR products from placental mRNA.
  
  
  RESULTS
  RFLP analysis showed that the IGF-II gene remains paternally expressed and the H19 gene remains maternally expressed in all placentas examined, independently of the birth weight status.
  
  
  CONCLUSIONS
  These results suggest that, in contrast with Beckwith-Wiedemann syndrome-associated macrosomia, loss of imprinting for IGF-II or H19 is not a common feature of diabetic pregnancies associated with macrosomia.
authors.affiliation: Department of Endocrinology and Diabetes, Marc Linquette Hospital, CHRU Lille, France. a-vambergue@chru-lille.fr
authors.forename: A
authors.initials: A
authors.lastname: Vambergue
authors.forename: I
authors.initials: I
authors.lastname: Fajardy
authors.forename: P
authors.initials: P
authors.lastname: Dufour
authors.forename: A S
authors.initials: AS
authors.lastname: Valat
authors.forename: M
authors.initials: M
authors.lastname: Vandersippe
authors.forename: P
authors.initials: P
authors.lastname: Fontaine
authors.forename: P M
authors.initials: PM
authors.lastname: Danze
authors.forename: J
authors.initials: J
authors.lastname: Rousseaux
mesh_terms: D004247:DNA / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005320:Fetal Macrosomia / Q000235:genetics*; D018392:Genomic Imprinting; D006801:Humans; D007231:Infant, Newborn; D007335:Insulin-Like Growth Factor II / Q000235:genetics* / Q000378:metabolism; D010920:Placenta / Q000737:chemistry / Q000378:metabolism*; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000235:genetics / Q000378:metabolism*; D062085:RNA, Long Noncoding; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D022661:RNA, Untranslated / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C094335:H19 long non-coding RNA; D062085:RNA, Long Noncoding; D012333:RNA, Messenger; D022661:RNA, Untranslated; D007335:Insulin-Like Growth Factor II; D004247:DNA