New insights into the roles of CUL1 in mouse placenta development.
CULLIN1
Placenta-specific
Placentation
Spongiotrophoblast
Journal
Biochemical and biophysical research communications
ISSN: 1090-2104
Titre abrégé: Biochem Biophys Res Commun
Pays: United States
ID NLM: 0372516
Informations de publication
Date de publication:
25 06 2021
25 06 2021
Historique:
received:
21
02
2021
accepted:
16
04
2021
pubmed:
3
5
2021
medline:
27
8
2021
entrez:
2
5
2021
Statut:
ppublish
Résumé
CULLIN1 (CUL1) protein, as a scaffold protein in Skp1-CUL1-F box (SCF) E3 ligases complex, was reported involved in different cellular functions to regulate the early embryonic development. In our previous study, we have demonstrated that CUL1 promote trophoblast cell invasion at the maternal-fetal interface in human and the CUL1 protein significantly decreased in preeclampsia (PE) placenta, but how CUL1 involved in placentation is still obscure. Due to the embryo lethal in CUL1 knockout mice, the lentivirus mediated placenta-specific CUL1 knockdown mice model was constructed to uncover the potential role of CUL1 in placentation. In this study, CUL1 was first detected in mouse placenta. CUL1 mainly expressed in trophoblast giant cell at E9.5, and spongiotrophoblast at E11.5 and E13.5 by using immunohistochemistry and int situ hybridization. In lentivirus mediated placenta specific mouse model, the number of implanted embryos was reduced in CUL1 shRNA group at E13.5 and E18.5 compared to control group. Based on the morphological analysis of histologic staining, we observed that spongiotrophoblast layer is expanded, fetal angiogenesis in labyrinth was obstructed and fetus blood cells were accumulated in vessels. These results indicated that decreased expression of CUL1 affect placentation of mice, which give new insights into the cause of gestational diseases, but the exactly mechanism still needs further study.
Identifiants
pubmed: 33933992
pii: S0006-291X(21)00675-6
doi: 10.1016/j.bbrc.2021.04.064
pii:
doi:
Substances chimiques
Cullin 1
0
Cullin Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
70-77Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.