PPARγ Expression Is Diminished in Macrophages of Recurrent Miscarriage Placentas

• Main Authors: Theresa Maria Kolben, Elisabeth Rogatsch, Aurelia Vattai, Anna Hester, Christina Kuhn, Elisa Schmoeckel, Sven Mahner, Udo Jeschke, Thomas Kolben
• Format: Article
• Language: English
• Published: MDPI AG 2018-06-01
• Series: International Journal of Molecular Sciences
• Subjects: PPARγ; first trimester placenta; decidual macrophages; miscarriage
• Online Access: http://www.mdpi.com/1422-0067/19/7/1872

PPARγ belongs to the group of nuclear receptors which is expressed in the trophoblast and together with other factors is responsible for the maintenance of pregnancy. Apart from that PPARγ is also a main factor for macrophage polarization. The aim of this study was to investigate the combined expression pattern and frequency of PPARγ under physiological circumstances and in spontaneous and recurrent miscarriages in the trophoblast and in maternal macrophages of the decidua. Human placental tissues of the first trimester (15 physiologic pregnancies, 15 spontaneous abortion and 16 recurrent miscarriage placentas) were analyzed for expression of the nuclear receptor PPARγ. Expression changes were evaluated by immunohistochemistry and real time PCR (RT-PCR) in trophoblast and in maternal macrophages of the decidua. Maternal macrophages were identified by double immunofluorescence using cluster of differentiation 68 (CD68) as marker for macrophages and further characterized regarding their M1/M2 polarization status. The intermediate villous trophoblast revealed a significantly lower PPARγ expression in spontaneous and recurrent abortion. Maternal macrophages express PPARγ. Their number is significantly enhanced in the decidua of spontaneous miscarriages whereas in recurrent miscarriages maternal macrophages seem to express PPARγ only in very few cases. PPARγ is associated with an M2 polarization state that is common for decidual macrophages. The lack of PPARγ in recurrent miscarriage decidual macrophages seems to be associated with a specific inflammatory response against the fetus.