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NLRP7 Plays A Functional Role in Regulating BMP4 Signaling During Differentiation of Patient-Derived Trophoblasts

View ORCID ProfileAybuke Alici-Garipcan, Burcu Özçimen, Ilke Suder, Volkan Ülker, View ORCID ProfileTamer T. Önder, Nesrin Özören
doi: https://doi.org/10.1101/850420
Aybuke Alici-Garipcan
Department of Molecular Biology and Genetics, Apoptosis and Cancer Immunology Laboratory (AKIL), Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey
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  • ORCID record for Aybuke Alici-Garipcan
Burcu Özçimen
School of Medicine, Koç University, Istanbul, Turkey
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Ilke Suder
Department of Molecular Biology and Genetics, Apoptosis and Cancer Immunology Laboratory (AKIL), Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey
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Volkan Ülker
Department of Obstetrics and Gynaecology, Oncology Unit, Kanuni Sultan Suleyman Training and Research Hospital, Istanbul, Turkey
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Tamer T. Önder
School of Medicine, Koç University, Istanbul, Turkey
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Nesrin Özören
Department of Molecular Biology and Genetics, Apoptosis and Cancer Immunology Laboratory (AKIL), Center for Life Sciences and Technologies, Bogazici University, Istanbul, Turkey
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  • For correspondence: nesrin.ozoren@boun.edu.tr
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Abstract

Complete Hydatidiform Mole (HM) is a gestational trophoblastic disease resulting in hyper proliferation of trophoblast cells and absence of embryo development. Mutations in the primate specific-maternal effect gene NLRP7 are the major cause of familial recurrent complete HM. Here, we established an in vitro model of HM using NLRP7 deficient patient-specific induced pluripotent stem cells (iPSCs) derived trophoblasts. Using whole transcriptome profiling during trophoblast differentiation, we showed that NLRP7 deficiency results in precocious downregulation of pluripotency factors, activation of trophoblast lineage markers and promotes maturation of differentiated extraembryonic cell types such as syncytiotrophoblasts. Interestingly, we found that these phenotypes are dependent on BMP4 signaling and BMP pathway inhibition corrected the excessive trophoblast differentiation of patient derived iPSCs. Our human iPSC model of a genetic placental disease recapitulates aspects of trophoblast biology, highlights the broad utility of iPSC-derived trophoblasts for modeling human placental diseases and identifies NLRP7 as an essential modulator of key developmental cell fate regulators.

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Posted November 24, 2019.
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NLRP7 Plays A Functional Role in Regulating BMP4 Signaling During Differentiation of Patient-Derived Trophoblasts
Aybuke Alici-Garipcan, Burcu Özçimen, Ilke Suder, Volkan Ülker, Tamer T. Önder, Nesrin Özören
bioRxiv 850420; doi: https://doi.org/10.1101/850420
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NLRP7 Plays A Functional Role in Regulating BMP4 Signaling During Differentiation of Patient-Derived Trophoblasts
Aybuke Alici-Garipcan, Burcu Özçimen, Ilke Suder, Volkan Ülker, Tamer T. Önder, Nesrin Özören
bioRxiv 850420; doi: https://doi.org/10.1101/850420

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