title: Transient CD15-positive endothelial phenotype in the human placenta correlates with physiological and pathological fetoplacental immaturity.
abstract: OBJECTIVE
  Placental growth and villous maturation are critical parameters of placental function at the end of pregnancy. A failure in these processes leads to the development of placental dysfunction, as well as fetal and neonatal mortality and morbidity. The aim of the study was to determine the relevant diagnostic markers associated with pathological placental development.
  
  
  METHODS
  Forty tissue samples from normal placentas of different gestational age and 68 pathological term placentas with defective villous maturation (GDM, idiopathic IUFD, preeclamsia, HELLP syndrome) comprised the comparative immunohistochemical study (CD15, CD45 and CD34). Positive immunohistochemical reactions were quantitatively assessed in the chorionic plate and vessels of the villi of different histological type.
  
  
  RESULTS
  Physiologically immature placentas of the first and second trimester and pathologically immature term placentas were characterized by marked endothelial CD15-immunostaining. A significant loss of CD15-positive endothelium of the placentas was associated with a physiological and accelerated villous maturity. A spatio-temporal correlation was shown for CD15+ endothelial cells (ECs) and the number of CD45+ stromal cells (SCs). A negative temporal correlation was shown for CD15+ ECs and CD15+ myelomonocytes in the fetal blood. CD34 expression in the ECs was stable during the pregnancy.
  
  
  CONCLUSIONS
  A correlation between a transient CD15-positive endothelial phenotype and a physiological and pathological fetoplacental immaturity was demonstrated. Physiological and accelerated placental maturation was accompanied by a significant disappearance of CD15-positive endothelium. We propose that "immature" CD15+ endothelium is an important diagnostic marker of the physiological and pathological fetoplacental immaturity.
authors.affiliation: Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany. Electronic address: larissa.seidmann@mail.ru.
authors.forename: L
authors.initials: L
authors.lastname: Seidmann
authors.affiliation: Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Suhan
authors.affiliation: Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany.
authors.forename: R
authors.initials: R
authors.lastname: Unger
authors.affiliation: Pediatric Clinic, Johann Wolfgang Goethe University, Frankfurt/Main, Germany.
authors.forename: V
authors.initials: V
authors.lastname: Gerein
authors.affiliation: Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany.
authors.forename: C J
authors.initials: CJ
authors.lastname: Kirkpatrick
mesh_terms: D000328:Adult; D018952:Antigens, CD34 / Q000378:metabolism*; D016022:Case-Control Studies; D016640:Diabetes, Gestational / Q000378:metabolism; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism*; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism; D005647:Fucosyltransferases / Q000378:metabolism*; D005865:Gestational Age; D017359:HELLP Syndrome / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D017493:Leukocyte Common Antigens / Q000378:metabolism*; D016256:Lewis X Antigen / Q000378:metabolism*; D010920:Placenta / Q000166:cytology / Q000378:metabolism; D010929:Placentation; D011225:Pre-Eclampsia / Q000378:metabolism; D011247:Pregnancy
chemical_list: D018952:Antigens, CD34; D016256:Lewis X Antigen; C066693:FUT4 protein, human; D005647:Fucosyltransferases; D017493:Leukocyte Common Antigens; C516769:PTPRC protein, human
keywords: CD15; Diagnostic marker; Endothelium; Hematopoiesis; Placental pathologies; Villous immaturity