Journal
NATURE COMMUNICATIONS
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms3311
Keywords
-
Categories
Funding
- Cardiff University LINK Award
- School of Psychology, Cardiff University
- BBSRC [BB/I014594/1, BB/D01235X/1] Funding Source: UKRI
- MRC [MC_UU_12012/4] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/B50118X/2, BB/I014594/1, BB/D01235X/1, BB/B50118X/1] Funding Source: researchfish
- British Heart Foundation [FS/09/029/27902] Funding Source: researchfish
- Medical Research Council [G0801418B] Funding Source: researchfish
Ask authors/readers for more resources
Imprinted, maternally silenced insulin-like growth factor-2 is expressed in both the foetus and placenta and has been shown to have roles in foetal and placental development in animal models. Here we compared mice engineered to be null for the placenta-specific P0 transcript (insulin-like growth factor-2-P0 KO) to mice with disruptions of all four insulin-like growth factor-2 transcripts, and therefore null for insulin-like growth factor-2 in both placenta and foetus (insulin-like growth factor-2-total KO). Both models lead to intrauterine growth restriction but dissociate between a situation where there is an imbalance between foetal demand and placental supply of nutrients (the insulin-like growth factor-2-P0 KO) and one where demand and supply is more balanced (the insulin-like growth factor-2-total KO). Increased reactivity to anxiety-provoking stimuli is manifested later in life only in those animals where there is a mismatch between placental supply and foetal demand for nutrients during gestation. Our findings further distinguish placental dysfunction from intrauterine growth restriction and reveal a role for the placenta in long-term programming of emotional behaviour.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available