@article{MTMT:30706654, title = {The prediction of early preeclampsia: Results from a longitudinal proteomics study. Results from a longitudinal proteomics study.}, url = {https://m2.mtmt.hu/api/publication/30706654}, author = {Tarca, Adi L and Romero, Roberto and Benshalom-Tirosh, Neta and Than, Nándor Gábor and Gudicha, Dereje W and Done, Bogdan and Pacora, Percy and Chaiworapongsa, Tinnakorn and Panaitescu, Bogdan and Tirosh, Dan and Gomez-Lopez, Nardhy and Draghici, Sorin and Hassan, Sonia S and Erez, Offer}, doi = {10.1371/journal.pone.0217273}, journal-iso = {PLOS ONE}, journal = {PLOS ONE}, volume = {14}, unique-id = {30706654}, issn = {1932-6203}, abstract = {To identify maternal plasma protein markers for early preeclampsia (delivery <34 weeks of gestation) and to determine whether the prediction performance is affected by disease severity and presence of placental lesions consistent with maternal vascular malperfusion (MVM) among cases.This longitudinal case-control study included 90 patients with a normal pregnancy and 33 patients with early preeclampsia. Two to six maternal plasma samples were collected throughout gestation from each woman. The abundance of 1,125 proteins was measured using high-affinity aptamer-based proteomic assays, and data were modeled using linear mixed-effects models. After data transformation into multiples of the mean values for gestational age, parsimonious linear discriminant analysis risk models were fit for each gestational-age interval (8-16, 16.1-22, 22.1-28, 28.1-32 weeks). Proteomic profiles of early preeclampsia cases were also compared to those of a combined set of controls and late preeclampsia cases (n = 76) reported previously. Prediction performance was estimated via bootstrap.We found that 1) multi-protein models at 16.1-22 weeks of gestation predicted early preeclampsia with a sensitivity of 71% at a false-positive rate (FPR) of 10%. High abundance of matrix metalloproteinase-7 and glycoprotein IIbIIIa complex were the most reliable predictors at this gestational age; 2) at 22.1-28 weeks of gestation, lower abundance of placental growth factor (PlGF) and vascular endothelial growth factor A, isoform 121 (VEGF-121), as well as elevated sialic acid binding immunoglobulin-like lectin 6 (siglec-6) and activin-A, were the best predictors of the subsequent development of early preeclampsia (81% sensitivity, FPR = 10%); 3) at 28.1-32 weeks of gestation, the sensitivity of multi-protein models was 85% (FPR = 10%) with the best predictors being activated leukocyte cell adhesion molecule, siglec-6, and VEGF-121; 4) the increase in siglec-6, activin-A, and VEGF-121 at 22.1-28 weeks of gestation differentiated women who subsequently developed early preeclampsia from those who had a normal pregnancy or developed late preeclampsia (sensitivity 77%, FPR = 10%); 5) the sensitivity of risk models was higher for early preeclampsia with placental MVM lesions than for the entire early preeclampsia group (90% versus 71% at 16.1-22 weeks; 87% versus 81% at 22.1-28 weeks; and 90% versus 85% at 28.1-32 weeks, all FPR = 10%); and 6) the sensitivity of prediction models was higher for severe early preeclampsia than for the entire early preeclampsia group (84% versus 71% at 16.1-22 weeks).We have presented herein a catalogue of proteome changes in maternal plasma proteome that precede the diagnosis of preeclampsia and can distinguish among early and late phenotypes. The sensitivity of maternal plasma protein models for early preeclampsia is higher in women with underlying vascular placental disease and in those with a severe phenotype.}, year = {2019}, eissn = {1932-6203} } @article{MTMT:30338008, title = {Minimal information for studies of extracellular vesicles 2018 (MISEV2018): a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines}, url = {https://m2.mtmt.hu/api/publication/30338008}, author = {Théry, C. and Witwer, K.W. and Aikawa, E. and Alcaraz, M.J. and Anderson, J.D. and Andriantsitohaina, R. and Antoniou, A. and Arab, T. and Archer, F. and Atkin-Smith, G.K. and Ayre, D.C. and Bach, J.-M. and Bachurski, D. and Baharvand, H. and Balaj, L. and Baldacchino, S. and Bauer, N.N. and Baxter, A.A. and Bebawy, M. and Beckham, C. and Bedina, Zavec A. and Benmoussa, A. and Berardi, A.C. and Bergese, P. and Bielska, E. and Blenkiron, C. and Bobis-Wozowicz, S. and Boilard, E. and Boireau, W. and Bongiovanni, A. and Borràs, F.E. and Bosch, S. and Boulanger, C.M. and Breakefield, X. and Breglio, A.M. and Brennan, M.Á. and Brigstock, D.R. and Brisson, A. and Broekman, M.L.D. and Bromberg, J.F. and Bryl-Górecka, P. and Buch, S. and Buck, A.H. and Burger, D. and Busatto, S. and Buschmann, D. and Bussolati, B. and Buzás, Edit Irén and Byrd, J.B. and Camussi, G. and Carter, D.R.F. and Caruso, S. and Chamley, L.W. and Chang, Y.-T. and Chaudhuri, A.D. and Chen, C. and Chen, S. and Cheng, L. and Chin, A.R. and Clayton, A. and Clerici, S.P. and Cocks, A. and Cocucci, E. and Coffey, R.J. and Cordeiro-da-Silva, A. and Couch, Y. and Coumans, F.A.W. and Coyle, B. and Crescitelli, R. and Criado, M.F. and D’Souza-Schorey, C. and Das, S. and de, Candia P. and De, Santana E.F. Jr. and De, Wever O. and del, Portillo H.A. and Demaret, T. and Deville, S. and Devitt, A. and Dhondt, B. and Di, Vizio D. and Dieterich, L.C. and Dolo, V. and Dominguez, Rubio A.P. and Dominici, M. and Dourado, M.R. and Driedonks, T.A.P. and Duarte, F.V. and Duncan, H.M. and Eichenberger, R.M. and Ekström, K. and EL, Andaloussi S. and Elie-Caille, C. and Erdbrügger, U. and Falcón-Pérez, J.M. and Fatima, F. and Fish, J.E. and Flores-Bellver, M. and Försönits, András and Frelet-Barrand, A. and Fricke, F. and Fuhrmann, G. and Gabrielsson, S. and Gámez-Valero, A. and Gardiner, C. and Gärtner, K. and Gaudin, R. and Gho, Y.S. and Giebel, B. and Gilbert, C. and Gimona, M. and Giusti, I. and Goberdhan, D.C.I. and Görgens, A. and Gorski, S.M. and Greening, D.W. and Gross, J.C. and Gualerzi, A. and Gupta, G.N. and Gustafson, D. and Handberg, A. and Haraszti, R.A. and Harrison, P. and Hegyesi, Hargita and Hendrix, A. and Hill, A.F. and Hochberg, F.H. and Hoffmann, K.F. and Holder, B. and Holthofer, H. and Hosseinkhani, B. and Hu, G. and Huang, Y. and Huber, V. and Hunt, S. and Ibrahim, A.G.-E. and Ikezu, T. and Inal, J.M. and Isin, M. and Ivanova, A. and Jackson, H.K. and Jacobsen, S. and Jay, S.M. and Jayachandran, M. and Jenster, G. and Jiang, L. and Johnson, S.M. and Jones, J.C. and Jong, A. and Jovanovic-Talisman, T. and Jung, S. and Kalluri, R. and Kano, S.-I. and Kaur, S. and Kawamura, Y. and Keller, E.T. and Khamari, Delaram and Khomyakova, E. and Khvorova, A. and Kierulf, P. and Kim, K.P. and Kislinger, T. and Klingeborn, M. and Klinke, D.J. II and Kornek, M. and Kosanović, M.M. and Kovács, Árpád Ferenc and Krämer-Albers, E.-M. and Krasemann, S. and Krause, M. and Kurochkin, I.V. and Kusuma, G.D. and Kuypers, S. and Laitinen, S. and Langevin, S.M. and Languino, L.R. and Lannigan, J. and Lässer, C. and Laurent, L.C. and Lavieu, G. and Lázaro-Ibáñez, E. and Le, Lay S. and Lee, M.-S. and Lee, Y.X.F. and Lemos, D.S. and Lenassi, M. and Leszczynska, A. and Li, I.T.S. and Liao, K. and Libregts, S.F. and Ligeti, Erzsébet and Lim, R. and Lim, S.K. and Linē, A. and Linnemannstöns, K. and Llorente, A. and Lombard, C.A. and Lorenowicz, M.J. and Lőrincz, Márton Ákos and Lötvall, J. and Lovett, J. and Lowry, M.C. and Loyer, X. and Lu, Q. and Lukomska, B. and Lunavat, T.R. and Maas, S.L.N. and Malhi, H. and Marcilla, A. and Mariani, J. and Mariscal, J. and Martens-Uzunova, E.S. and Martin-Jaular, L. and Martinez, M.C. and Martins, V.R. and Mathieu, M. and Mathivanan, S. and Maugeri, M. and McGinnis, L.K. and McVey, M.J. and Meckes, D.G. Jr and Meehan, K.L. and Mertens, I. and Minciacchi, V.R. and Möller, A. and Møller, Jørgensen M. and Morales-Kastresana, A. and Morhayim, J. and Mullier, F. and Muraca, M. and Musante, L. and Mussack, V. and Muth, D.C. and Myburgh, K.H. and Najrana, T. and Nawaz, M. and Nazarenko, I. and Nejsum, P. and Neri, C. and Neri, T. and Nieuwland, R. and Nimrichter, L. and Nolan, J.P. and Nolte-’t, Hoen E.N.M. and Hooten, N.N. and O’Driscoll, L. and O’Grady, T. and O’Loghlen, A. and Ochiya, T. and Olivier, M. and Ortiz, A. and Ortiz, L.A. and Osteikoetxea, Xabier and Ostegaard, O. and Ostrowski, M. and Park, J. and Pegtel, D.M. and Peinado, H. and Perut, F. and Pfaffl, M.W. and Phinney, D.G. and Pieters, B.C.H. and Pink, R.C. and Pisetsky, D.S. and Pogge, von Strandmann E. and Polakovicova, I. and Poon, I.K.H. and Powell, B.H. and Prada, I. and Pulliam, L. and Quesenberry, P. and Radeghieri, A. and Raffai, R.L. and Raimondo, S. and Rak, J. and Ramirez, M.I. and Raposo, G. and Rayyan, M.S. and Regev-Rudzki, N. and Ricklefs, F.L. and Robbins, P.D. and Roberts, D.D. and Rodrigues, S.C. and Rohde, E. and Rome, S. and Rouschop, K.M.A. and Rughetti, A. and Russell, A.E. and Saá, P. and Sahoo, S. and Salas-Huenuleo, E. and Sánchez, C. and Saugstad, J.A. and Saul, M.J. and Schiffelers, R.M. and Schneider, R. and Schøyen, T.H. and Scott, A. and Shahaj, E. and Sharma, S. and Shatnyeva, O. and Shekari, F. and Shelke, G.V. and Shetty, A.K. and Shiba, K. and Siljander, P.R.-M. and Silva, A.M. and Skowronek, A. and Snyder, O.L. II and Soares, R.P. and Sódar, Barbara and Soekmadji, C. and Sotillo, J. and Stahl, P.D. and Stoorvogel, W. and Stott, S.L. and Strasser, E.F. and Swift, S. and Tahara, H. and Tewari, M. and Timms, K. and Tiwari, S. and Tixeira, R. and Tkach, M. and Toh, W.S. and Tomasini, R. and Torrecilhas, A.C. and Tosar, J.P. and Toxavidis, V. and Urbanelli, L. and Vader, P. and van, Balkom B.W.M. and van, der Grein S.G. and Van, Deun J. and van, Herwijnen M.J.C. and Van, Keuren-Jensen K. and van, Niel G. and van, Royen M.E. and van, Wijnen A.J. and Vasconcelos, M.H. and Vechetti, I.J. Jr and Veit, T.D. and Vella, L.J. and Velot, É. and Verweij, F.J. and Vestad, B. and Viñas, J.L. and Visnovitz, Tamás and Visnovitzné Dr Vukman, Krisztina and Wahlgren, J. and Watson, D.C. and Wauben, M.H.M. and Weaver, A. and Webber, J.P. and Weber, V. and Wehman, A.M. and Weiss, D.J. and Welsh, J.A. and Wendt, S. and Wheelock, A.M. and Wiener, Zoltán and Witte, L. and Wolfram, J. and Xagorari, A. and Xander, P. and Xu, J. and Yan, X. and Yáñez-Mó, M. and Yin, H. and Yuana, Y. and Zappulli, V. and Zarubova, J. and Žėkas, V. and Zhang, J.-Y. and Zhao, Z. and Zheng, L. and Zheutlin, A.R. and Zickler, A.M. and Zimmermann, P. and Zivkovic, A.M. and Zocco, D. and Zuba-Surma, E.K.}, doi = {10.1080/20013078.2018.1535750}, journal-iso = {J EXTRACELLULAR VESICL}, journal = {JOURNAL OF EXTRACELLULAR VESICLES}, volume = {7}, unique-id = {30338008}, year = {2018}, eissn = {2001-3078}, orcid-numbers = {Buzás, Edit Irén/0000-0002-3744-206X; Försönits, András/0000-0002-9298-8890; Hegyesi, Hargita/0000-0002-8800-5169; Kovács, Árpád Ferenc/0000-0002-7742-160X; Ligeti, Erzsébet/0000-0001-6374-729X; Lőrincz, Márton Ákos/0000-0002-2819-5116; Osteikoetxea, Xabier/0000-0003-3628-0174; Sódar, Barbara/0000-0002-8803-7304; Visnovitz, Tamás/0000-0002-7962-5083; Wiener, Zoltán/0000-0001-7056-4926} } @article{MTMT:3273020, title = {Various levels of circulating exosomal total-miRNA and miR-210 hypoxamiR in different forms of pregnancy hypertension}, url = {https://m2.mtmt.hu/api/publication/3273020}, author = {Biró, Orsolya and Alasztics, Bálint and Molvarec, Attila and Joó, József Gábor and Nagy, Bálint and Rigó, János}, doi = {10.1016/j.preghy.2017.09.002}, journal-iso = {PREGNANCY HYPERTENS}, journal = {PREGNANCY HYPERTENSION}, volume = {10}, unique-id = {3273020}, issn = {2210-7789}, abstract = {Introduction: Hypertension is a common complication during pregnancy, affecting 10% of pregnant women worldwide. Several microRNA (miRNA) were shown to be involved in hypertensive disorders of pregnancy. In preeclampsia (PE), placental dysfunction causes the enhanced release of extracellular vesicle-derived miRNAs. The hypoxia-sensitive hsa-mir-210 is the most common PE-associated miRNA, but its exosomal profile has not been investigated. Objectives: Our aims were to measure exosomal total-miRNA concentration and to perform expression analysis of circulating exosomal hsa-miR-210 in women affected by chronic hypertension (CHT) gestational hypertension (GHT) or PE. Materials and methods: We collected plasma samples from women with CHT, GHT, PE (moderate: mPE and severe: sPE) and from normotensive pregnancies. Exosomal miRNAs were extracted and miRNA concentration was measured. RT-PCR was carried out with hsa-miR-210-3p-specific primers and relative expression was calculated using the comparative Ct method. Results: The total-miRNA concentration was different in the disease subgroups, and was significantly higher in mPE and sPE compared to the other groups. We found a significant difference in the relative exosomal hsa-miR-210-3p expression between all hypertensive groups compared to the normotensive samples, but significant upregulation was only observed in case of mPE and sPE patients. Both the level of total-miRNA and hsa-miR-210 expression was higher in case of severe PE. Conclusions: The level of circulating exosomal total-miRNA and hsa-miR-210 was elevated in women with PE, and it was higher in the severe form. We showed that hsa-miR-210 is secreted via exosomes, which may have a role in the pathomechanism of the disease. © 2017 International Society for the Study of Hypertension in Pregnancy.}, keywords = {PREECLAMPSIA; microRNA; exosome; Maternal circulation}, year = {2017}, eissn = {2210-7797}, pages = {207-212}, orcid-numbers = {Biró, Orsolya/0000-0002-4300-3602; Alasztics, Bálint/0000-0002-4011-8439; Molvarec, Attila/0000-0002-3229-3034; Joó, József Gábor/0000-0001-9820-6514; Nagy, Bálint/0000-0002-0295-185X; Rigó, János/0000-0003-2762-6516} }