Expression Patterns of Two Serine Protease HtrA1 Forms in Human Placentas Complicated by Preeclampsia with and without Intrauterine Growth Restriction |
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| Authors: | T. Lorenzi D. Marzioni S. Giannubilo A. Quaranta C. Crescimanno A. De Luca A. Baldi T. Todros A.L. Tranquilli M. Castellucci |
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| Affiliation: | 1. Department of Molecular Biology and Cell Pathology, Third Faculty of Medicine, Charles University, Prague, Czech Republic;2. Institute for the Care of the Mother and Child, Third Faculty of Medicine, Charles University, Prague, Czech Republic;1. Department of Molecular Biology and Cell Pathology, Third Faculty of Medicine, Charles University, Prague, Czech Republic;2. Institute for the Care of the Mother and Child, Third Faculty of Medicine, Charles University, Prague, Czech Republic;1. Department of Geriatrics, Neurosciences and Orthopedics, Catholic University of the Sacred Heart, L.go A. Gemelli 8, 00168 Rome, Italy;2. Department of Experimental and Clinical Medicine, Section of Neuroscience and Cell Biology, School of Medicine, Università Politecnica delle Marche, Via Tronto 10/a, 60020 Ancona, Italy;3. Unit of Clinical and Molecular Epidemiology, IRCCS San Raffaele Pisana, Via di Val Cannuta, 247, 00166 Rome, Italy;4. DICOMOSA Group, Department of Psychology, Area of Psychobiology, University of A Coruña, Campus A Coruña, E15071 A Coruña, Spain;1. Department of Experimental and Clinical Medicine, Università Politecnica delle Marche, 60126 Ancona, Italy;2. Department of Biomedical and Surgical Science, Clinic of Obstetrics and Gynaecology, University of Perugia, 06132 Perugia, Italy;3. Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, 60126 Ancona, Italy;4. Fondazione Policlinico Universitario A. Gemelli IRCCS, U.O.C. di Ostetricia e Patologia Ostetrica, Dipartimento di Scienze della Salute della Donna, del Bambino e di Sanità Pubblica, 00168 Roma, Italy;5. Centre of Perinatal and Reproductive Medicine, University of Perugia, Italy;6. Department of Clinical Sciences, Università Politecnica delle Marche, Salesi Hospital, 60123 Ancona, Italy;7. Università Cattolica del Sacro Cuore, Istituto di Clinica Ostetrica e Ginecologica, 00168 Roma, Italy;8. Department of Obstetrics and Gynaecology I.M. Sechenov First State University, Moscow, Russia;9. Centre of Epidemiology and Biostatistics, Università Politecnica delle Marche, 60126 Ancona, Italy;10. Center of Clinical Pathology and Innovative Therapy, IRCCS INRCA National Institute, 60100 Ancona, Italy |
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| Abstract: | Preeclampsia (PE) and intrauterine growth restriction (IUGR) are pregnancy-specific disorders that have in common abnormal placental implantation, a marked proliferation of villous cytotrophoblastic cells and focal necrosis of the syncytiotrophoblast. Several studies show an ischemic placenta with a high-resistance vasculature, which cannot deliver an adequate blood supply to the feto-placental unit. The cause of PE is a matter of debate, but recently studies in mice suggest that the primary feto-placental lesions are sufficient to initiate the disease.HtrA1, a member of the family of HtrA proteins, is a secreted multidomain protein with serine protease activity. It is expressed in first and third trimester of gestation. In specimens from the first trimester of gestation, immunostaining for HtrA1 is generally found in both layers of villous trophoblast, syncytiotrophoblast and cytotrophoblast. Cytoplasm of extravillous trophoblast and extracellular matrix of cell islands and cell columns are labeled for HtrA1. Specimens from third trimester of gestation show a more intense positivity for HtrA1 in the syncytiotrophoblast than in cytotrophoblast. The extravillous trophoblast and the decidual cells, is positive for HtrA1. The purpose of this study is to investigate the expression pattern of HtrA1 in placentas from PE without IUGR (maternal PE) and with IUGR (fetal PE) by quantitative western blotting and immunohistochemistry. By quantitative western blotting analysis we observed a significant upregulation of ～30 kDa HtrA1 form in PE. Differently, we detected a significant total HtrA1 down-regulation in PE–IUGR. Moreover, immunostaining for HtrA1 was positive in the villous trophoblast, in the syncytial knots and irregularly in the fetal vessel walls in PE placentas while immunostaining for HtrA1was present particularly in the syncytial knots in PE–IUGR placentas. In conclusion, we suggest that the ～30 kDa HtrA1 form can be correlated to maternal PE while that the significant down-regulation of total HtrA1 can be correlated to placental PE. These HtrA1 alterations could be considered as possible markers to discriminate placental PE from maternal PE. |
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