TY  - JOUR
A1  - Wildner, Julia Maria
A1  - Friemel, Alexandra
A1  - Jennewein, Lukas
A1  - Roth, Susanne
A1  - Ritter, Andreas Hans
A1  - Schüttler, Cornelia
A1  - Chen, Qi
A1  - Louwen, Frank
A1  - Yuan, Juping
A1  - Kreis, Nina-Naomi
T1  - RITA is expressed in trophoblastic cells and is involved in differentiation processes of the placenta
T2  - Cells
N2  - Preeclampsia (PE) remains a leading cause of maternal and perinatal mortality and morbidity worldwide. Its pathogenesis has not been fully elucidated and no causal therapy is currently available. It is of clinical relevance to decipher novel molecular biomarkers. RITA (RBP-J (recombination signal binding protein J)-interacting and tubulin-associated protein) has been identified as a negative modulator of the Notch pathway and as a microtubule-associated protein important for cell migration and invasion. In the present work, we have systematically studied RITA’s expression in primary placental tissues from patients with early- and late-onset PE as well as in various trophoblastic cell lines. RITA is expressed in primary placental tissues throughout gestation, especially in proliferative villous cytotrophoblasts, in the terminally differentiated syncytiotrophoblast, and in migrating extravillous trophoblasts. RITA’s messenger RNA (mRNA) level is decreased in primary tissue samples from early-onset PE patients. The deficiency of RITA impairs the motility and invasion capacity of trophoblastic cell lines, and compromises the fusion ability of trophoblast-derived choriocarcinoma cells. These data suggest that RITA may play important roles in the development of the placenta and possibly in the pathogenesis of PE.
KW  - RITA
KW  - preeclampsia
KW  - trophoblasts
KW  - motility
KW  - invasion
KW  - fusion
Y1  - 2019
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/51656
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-516561
SN  - 2073-4409
N1  - This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
VL  - 8
IS  - 12, Art. 1484
SP  - 1
EP  - 18
PB  - MDPI
CY  - Basel
ER  -