Kiss1 mutant placentas show normal structure and function in the mouse

- The structure and function of Kiss1 and Gpr54 mutant placentas was examined in transgenic mice.
- Kiss1 and Gpr54 mutant placentas are not associated with fetal loss during gestation or reduced pup weight at birth.
- Kiss1 mutant placentas show normal structural components.
- Kiss1 mutant placentas show normal transport of glucose and amino-acids.

IntroductionKisspeptins, 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.MethodsWe have used Kiss1 and Gpr54 mutant mice to investigate the role of kisspeptin signaling in the structure and function of the mouse placenta.ResultsExpression 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.DiscussionThese data indicate that mouse placentas can develop a normal structure and function without kisspeptin signaling and can support normal fetal development and growth.