globalchange  > 气候变化与战略
DOI: 10.1073/pnas.1920201117
论文题名:
Atypical protein kinase C iota (PKC?/?) ensures mammalian development by establishing the maternal-fetal exchange interface
作者: Bhattacharya B.; Home P.; Home P.; Ganguly A.; Ray S.; Ghosh A.; Islam M.R.; French V.; French V.; Marsh C.; Marsh C.; Gunewardena S.; Okae H.; Arima T.; Paul S.; Paul S.; Paul S.
刊名: Proceedings of the National Academy of Sciences of the United States of America
ISSN: 0027-8424
出版年: 2020
卷: 117, 期:25
起始页码: 14280
结束页码: 14291
语种: 英语
英文关键词: Cytotrophoblast ; Human trophoblast stem cell ; Placenta ; Protein kinase Cγ/ι ; Syncytiotrophoblast
Scopus关键词: peroxisome proliferator activated receptor gamma ; protein kinase C iota ; transcription factor ; transcription factor GATA 2 ; transcription factor GCM1 ; unclassified drug ; DNA binding protein ; GATA2 protein, human ; Gata2 protein, mouse ; GCM1 protein, human ; Gcm1 protein, mouse ; isoenzyme ; peroxisome proliferator activated receptor gamma ; protein kinase C ; protein kinase C lambda ; transcription factor ; transcription factor GATA 2 ; animal cell ; animal tissue ; Article ; cell death ; cell differentiation ; cell maturation ; controlled study ; embryo ; female ; first trimester pregnancy ; human ; human cell ; human tissue ; in vitro study ; mother fetus relationship ; mouse ; nonhuman ; placenta development ; priority journal ; protein depletion ; protein expression ; protein function ; signal transduction ; stem cell ; syncytiotrophoblast cell ; transplantation ; trophoblast ; animal ; animal model ; cytology ; fetomaternal transfusion ; genetics ; knockout mouse ; male ; metabolism ; physiology ; placenta ; pregnancy ; Animals ; Cell Differentiation ; DNA-Binding Proteins ; Female ; GATA2 Transcription Factor ; Humans ; Isoenzymes ; Male ; Maternal-Fetal Exchange ; Mice ; Mice, Knockout ; Models, Animal ; Placenta ; Placentation ; PPAR gamma ; Pregnancy ; Protein Kinase C ; Signal Transduction ; Stem Cells ; Transcription Factors ; Trophoblasts
英文摘要: In utero mammalian development relies on the establishment of the maternal-fetal exchange interface, which ensures transportation of nutrients and gases between the mother and the fetus. This exchange interface is established via development of multinucleated syncytiotrophoblast cells (SynTs) during placentation. In mice, SynTs develop via differentiation of the trophoblast stem cell-like progenitor cells (TSPCs) of the placenta primordium, and in humans, SynTs are developed via differentiation of villous cytotrophoblast (CTB) progenitors. Despite the critical need in pregnancy progression, conserved signaling mechanisms that ensure SynT development are poorly understood. Herein, we show that atypical protein kinase C iota (PKCγ/ι) plays an essential role in establishing the SynT differentiation program in trophoblast progenitors. Loss of PKCγ/ι in the mouse TSPCs abrogates SynT development, leading to embryonic death at approximately embryonic day 9.0 (E9.0).We also show that PKCγ/ι-mediated priming of trophoblast progenitors for SynT differentiation is a conserved event during human placentation. PKCγ/ι is selectively expressed in the first-trimester CTBs of a developing human placenta. Furthermore, loss of PKCγ/ι in CTB-derived human trophoblast stem cells (human TSCs) impairs their SynT differentiation potential both in vitro and after transplantation in immunocompromised mice. Our mechanistic analyses indicate that PKCγ/ι signaling maintains expression of GCM1, GATA2, and PPARγ, which are key transcription factors to instigate SynT differentiation programs in both mouse and human trophoblast progenitors. Our study uncovers a conserved molecular mechanism, in which PKCγ/ι signaling regulates establishment of the maternal-fetal exchange surface by promoting trophoblast progenitor-to-SynT transition during placentation. © 2020 National Academy of Sciences. All rights reserved.
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资源类型: 期刊论文
标识符: http://119.78.100.158/handle/2HF3EXSE/163459
Appears in Collections:气候变化与战略

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作者单位: Bhattacharya, B., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; Home, P., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States, Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States; Home, P., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States, Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States; Ganguly, A., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; Ray, S., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; Ghosh, A., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; Islam, M.R., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States; French, V., Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; French, V., Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Marsh, C., Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Marsh, C., Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Gunewardena, S., Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Okae, H., Department of Informative Genetics, Environment and Genome Research Center, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan; Arima, T., Department of Informative Genetics, Environment and Genome Research Center, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan; Paul, S., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States, Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Paul, S., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States, Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States; Paul, S., Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160, United States, Institute for Reproduction and Perinatal Research, University of Kansas Medical Center, Kansas City, KS 66160, United States, Department of Obstetrics and Gynecology, University of Kansas Medical Center, Kansas City, KS 66160, United States

Recommended Citation:
Bhattacharya B.,Home P.,Home P.,et al. Atypical protein kinase C iota (PKC?/?) ensures mammalian development by establishing the maternal-fetal exchange interface[J]. Proceedings of the National Academy of Sciences of the United States of America,2020-01-01,117(25)
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