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Kiss1 mutant placentas show normal structure and function in the mouse.


Type

Article

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Authors

Herreboudt, AM 
Kyle, VRL 
Lawrence, J 
Doran, J 
Colledge, WH 

Abstract

INTRODUCTION: Kisspeptins, encoded by the Kiss1 gene, are a set of related neuropeptides that are required for activation of the mammalian reproductive axis at puberty and to maintain fertility. In addition, kisspeptin signaling via the G-protein coupled receptor GPR54 (KISS1R) has been suggested to regulate human placental formation and correlations have been found between altered kisspeptin levels in the maternal blood and the development of pre-eclampsia. METHODS: We have used Kiss1 and Gpr54 mutant mice to investigate the role of kisspeptin signaling in the structure and function of the mouse placenta. RESULTS: Expression of Kiss1 and Gpr54 was confirmed in the mouse placenta but no differences in birth weight were found in mice that had been supported by a mutant placenta during fetal development. Stereological measurements found no differences between Kiss1 mutant and wild-type placentas. Measurement of amino-acid and glucose transport across the Kiss1 mutant placentas at E15.5 days did not reveal any functional defects. DISCUSSION: These data indicate that mouse placentas can develop a normal structure and function without kisspeptin signaling and can support normal fetal development and growth.

Description

Keywords

Gpr54/Kiss1r, Kiss1, Kisspeptin, Knock-out mice, Placental transport, Animals, Birth Weight, Female, Kisspeptins, Mice, Mice, Knockout, Placenta, Pregnancy, Receptors, G-Protein-Coupled, Receptors, Kisspeptin-1, Signal Transduction

Journal Title

Placenta

Conference Name

Journal ISSN

0143-4004
1532-3102

Volume Title

36

Publisher

Elsevier BV
Sponsorship
Biotechnology and Biological Sciences Research Council (BB/F01936X/1)
Biotechnology and Biological Sciences Research Council (BB/K003178/1)
This work was supported by the BBSRC (Grant number BB/F01936X/1), Alice Herreboudt was supported by a BBSRC CASE studentship in collaboration with Takeda Cambridge.