title: Activating protein-1 family of transcription factors in the human placenta complicated by preeclampsia with and without fetal growth restriction.
abstract: Preeclampsia (PE) is a serious disorder of human pregnancy, it is often associated with fetal growth restriction (FGR) which is a failure of the fetus to reach its own growth potential. Activator protein-1 (AP-1) is a family of transcription factors inducible in response to a variety of extracellular stimuli and functions. AP-1 plays a complex role in the regulation of different fundamental cellular processes, including cell proliferation, survival, death and transformation. We investigate the expression pattern of AP-1 transcription factors in normal placentas during gestation and in placentas from PE without and with FGR using semiquantitative RT-PCR and immunohistochemistry techniques. The most interesting data concern the alterations of protein expression patterns of c-fos, Jun D and c-jun in normal gestation as well as in PE and PE-FGR pathologies. In addition, alterations but not significant changes are detected in mRNA expressions for these transcription factors. We strongly suggest that c-fos is implicated in regulating invasiveness mechanism of extravillous trophoblast in normal gestation as well as in PE placentas. In addition, we suggest that the opposite modulation of Jun D and c-jun in PE and PE-FGR supports the recent hypothesis that PE and PE-FGR could be considered two pathologies with different origin (maternal and placental) each of which has a different molecular pattern of expression.
authors.affiliation: Department of Molecular Pathology and Innovative Therapies, Marche Polytechnic University, Via Tronto, 10/a - I-60126 Ancona, Italy. d.marzioni@univpm.it
authors.forename: D
authors.initials: D
authors.lastname: Marzioni
authors.forename: T
authors.initials: T
authors.lastname: Todros
authors.forename: S
authors.initials: S
authors.lastname: Cardaropoli
authors.forename: A
authors.initials: A
authors.lastname: Rolfo
authors.forename: T
authors.initials: T
authors.lastname: Lorenzi
authors.forename: P
authors.initials: P
authors.lastname: Ciarmela
authors.forename: R
authors.initials: R
authors.lastname: Romagnoli
authors.forename: L
authors.initials: L
authors.lastname: Paulesu
authors.forename: M
authors.initials: M
authors.lastname: Castellucci
mesh_terms: D000328:Adult; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007231:Infant, Newborn; D010920:Placenta / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000235:genetics / Q000378:metabolism*; D011247:Pregnancy; D016760:Proto-Oncogene Proteins c-fos / Q000235:genetics / Q000378:metabolism; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000378:metabolism; D012313:RNA / Q000737:chemistry / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018709:Statistics, Nonparametric; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000378:metabolism*; D055815:Young Adult
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1; D012313:RNA