Expression of inhibin/activin subunits alpha (-α), BetaA (-βA), and BetaB (-βB) in placental tissue of normal, preeclamptic, and HELLP pregnancies

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 α-subunit and one of two possible β-subunits (βA or βB). 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-α- and both β-subunits (βA- and βB-subunits) using double immunofluorescence technique. A significant lower expression of the inhibin-α subunit in preeclamptic and HELLP placental tissue compared to normal pregnancies was observed, while the inhibin-α immunostaining was significantly upregulated in syncytotrophoblast. Additionally, we demonstrated a significant down-regulation of inhibin-βB subunit in extravillous trophoblast cells between normal and preeclamptic compared to HELLP placental tissue, while inhibin-βA-subunit was significantly higher in preeclamptic syncytotrophoblast cells. A colocalization of inhibin-α 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 βB-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 βA-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.