IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise.
Animals
Antigens, Differentiation
/ immunology
Apoptosis Regulatory Proteins
/ immunology
Cell Fusion
Female
Fetal Death
/ etiology
Fetal Resorption
/ immunology
Gene Products, env
/ immunology
Humans
Interferon Type I
/ immunology
Intracellular Signaling Peptides and Proteins
/ immunology
Mice
Poly I-C
/ pharmacology
Pregnancy
Pregnancy Proteins
/ immunology
RNA-Binding Proteins
/ immunology
Trophoblasts
/ drug effects
Journal
Science (New York, N.Y.)
ISSN: 1095-9203
Titre abrégé: Science
Pays: United States
ID NLM: 0404511
Informations de publication
Date de publication:
12 07 2019
12 07 2019
Historique:
received:
25
01
2019
accepted:
23
05
2019
entrez:
13
7
2019
pubmed:
13
7
2019
medline:
24
3
2020
Statut:
ppublish
Résumé
Elevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in
Identifiants
pubmed: 31296770
pii: 365/6449/176
doi: 10.1126/science.aaw7733
doi:
Substances chimiques
Antigens, Differentiation
0
Apoptosis Regulatory Proteins
0
Gene Products, env
0
IFIT2 protein, human
0
IFIT3 protein, human
0
Interferon Type I
0
Intracellular Signaling Peptides and Proteins
0
Pregnancy Proteins
0
RNA-Binding Proteins
0
leu-13 antigen
0
syncytin
0
Poly I-C
O84C90HH2L
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
176-180Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.