title: Determination of cytokine mRNA-expression in term human placenta of patients with gestational hypertension, intrauterine growth retardation and gestational diabetes mellitus using polymerase chain reaction.
abstract: OBJECTIVE
  Our objective was to test the hypothesis, that pregnancy-related diseases are going along with changes in cytokine mRNA-expression at the placental site, either as a part of a pathological process or in connection with regulatory mechanisms induced by disturbances at the feto-maternal interface resulting from previous pathological changes--in the sense of counterregulation.
  
  
  METHODS
  The cytokines chosen for this investigation are known to 1.) be expressed in the human placental tissue, 2.) to be involved in immunological processes and 3.) the regulation of growth and differentiation processes of different cell types of the placenta or decidua, 4.) to play a role in the angiogenesis at the feto-placental interface and 5.) to be involved in pathological processes in other human diseases. 32 samples derived from term human placentas were examined for messenger RNA levels of interleukin 1 alpha (II-1 alpha), tumor necrosis factor-alpha (TNF-alpha), platelet derived growth factor-A chain (PDGF-A), platelet derived growth factor-B chain (PDGF-B), and platelet derived growth factor receptor (PDGF-R) using a semiquantitative reverse transcriptase (RT) polymerase chain reaction (PCR) protocol. To calibrate samples in our procedure, beta-actin mRNA (messenger ribonucleic acid) known as a "house keeping" gene was proven to be constantly expressed. The sample-groups consisted of normal pregnancies (n = 8), gestational hypertension (GH, n = 7), intrauterine growth retardation (IUGR, n = 6), gestational diabetes mellitus (GDM, n = 5), and gemini (n = 3 x 2).
  
  
  RESULTS
  Throughout the 32 samples, a significant correlation between PDGF-A and PDGF-R expression, PDGF-A and TNF-alpha expression was stated (p = 0.007). Compared with the pattern of expression in normal placentas, placentas of growth retarded pregnancies had higher Il-1 alpha mRNA (p = 0.016), PDGF-A (p = 0.029) and PDGF-B (p = 0.001) levels. The samples of the gestational hypertension group and placentas of patients with gestational diabetes displayed a significantly stronger PDGF-R mRNA signal (p = 0.0029 and p = 0.008).
  
  
  CONCLUSIONS
  Though these marked differences in cytokine mRNA levels between clinical groups were statistically proven, clear correlation of these differences with clinical data was not found.
authors.affiliation: Biochemical Institute of the University of Rostock. heinig@uni-muenster.de
authors.forename: J
authors.initials: J
authors.lastname: Heinig
authors.forename: S
authors.initials: S
authors.lastname: Wilhelm
authors.forename: H
authors.initials: H
authors.lastname: Müller
authors.forename: V
authors.initials: V
authors.lastname: Briese
authors.forename: T
authors.initials: T
authors.lastname: Bittorf
authors.forename: J
authors.initials: J
authors.lastname: Brock
mesh_terms: D000199:Actins / Q000235:genetics; D000328:Adult; D016022:Case-Control Studies; D016207:Cytokines / Q000235:genetics*; D016640:Diabetes, Gestational / Q000276:immunology*; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology*; D005786:Gene Expression Regulation; D006801:Humans; D066298:In Vitro Techniques; D007375:Interleukin-1 / Q000235:genetics; D010920:Placenta / Q000276:immunology*; D010922:Placenta Diseases / Q000276:immunology*; D010982:Platelet-Derived Growth Factor / Q000235:genetics; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000032:analysis; D017479:Receptors, Platelet-Derived Growth Factor / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D014427:Twins
chemical_list: D000199:Actins; D016207:Cytokines; D007375:Interleukin-1; D010982:Platelet-Derived Growth Factor; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D017479:Receptors, Platelet-Derived Growth Factor