title: Expression of inhibin/activin subunits alpha (-alpha), betaA (-betaA), and betaB (-betaB) in placental tissue of normal, preeclamptic, and HELLP pregnancies.
abstract: During human pregnancy the placenta produces a variety of proteins for the establishment of the fetoplacental unit, including inhibins and activins. Inhibins are dimeric glycoproteins, composed of an alpha-subunit and one of two possible beta-subunits (betaA or betaB). Aims of the present study were (a) the determination of the frequency and tissue distribution patterns of the inhibin/activin subunits in human placental tissue of normal pregnancies and pregnancies complicated with preeclampsia and HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and (b) the assessment of a combined expression of inhibin-alpha- and both beta-subunits (betaA-and betaB-subunits) using double immunofluorescence technique. A significant lower expression of the inhibin-alpha subunit in preeclamptic and HELLP placental tissue compared to normal pregnancies was observed, while the inhibin-alpha immunostaining was significantly upregulated in syncytotrophoblast. Additionally, we demonstrated a significant down-regulation of inhibin-betaB subunit in extravillous trophoblast cells between normal and preeclamptic compared to HELLP placental tissue, while inhibin-betaA-subunit was significantly higher in preeclamptic syncytotrophoblast cells. A colocalization of inhibin-alpha and the beta-subunits could be demonstrated, suggesting a production and secretion of intact inhibin A and inhibin B. Therefore, inhibin A and activin A might be useful markers in preeclampsia. Valuable parameters in HELLP syndrome could be inhibin A, rather than inhibin B, and activin B. Furthermore, the lower betaB-subunit production in extravillous trophoblast cells demonstrates that this subunit might have an important role in the pathogenesis of HELLP syndrome. Additionally, the higher production of the betaA-subunit in syncytotrophoblast cells suggest a higher production of activin A rather than inhibin A in preeclampsia that might be utilized as a marker of placental function.
authors.affiliation: 1st Department of Obstetrics and Gynecology, Ludwig-Maximilians-University Munich, Maistrasse 11, 80337 Munich, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Mylonas
authors.forename: B
authors.initials: B
authors.lastname: Schiessl
authors.forename: U
authors.initials: U
authors.lastname: Jeschke
authors.forename: J
authors.initials: J
authors.lastname: Vogl
authors.forename: A
authors.initials: A
authors.lastname: Makrigiannakis
authors.forename: C
authors.initials: C
authors.lastname: Kuhn
authors.forename: S
authors.initials: S
authors.lastname: Schulze
authors.forename: F
authors.initials: F
authors.lastname: Kainer
authors.forename: K
authors.initials: K
authors.lastname: Friese
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D017359:HELLP Syndrome / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007124:Immunoenzyme Techniques; D028322:Inhibin-beta Subunits / Q000378:metabolism*; D007265:Inhibins / Q000378:metabolism*; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy; D014327:Trophoblasts / Q000378:metabolism* / Q000473:pathology
chemical_list: D015415:Biomarkers; C094377:inhibin-alpha subunit; D007265:Inhibins; D028322:Inhibin-beta Subunits