The effect of embryo and maternal genotypes on prolificacy, intrauterine growth retardation and postnatal development of Nos3-knockout mice
Mice deficient for endothelial nitric oxide synthase (NOS3-/-) may represent a good model for studying embryo loss and intrauterine growth retardation caused by vascular deficiencies. We determined the effects of embryo genotype (homozygous vs. heterozygous descendants with paternal or maternal source of the non-functional NOS3 allele) and maternal environment (NOS3-/- vs. wild-type NOS3+/+ females) on the appearance of estrus, fertility and prolificacy rates and live weight in the first week of life as well as phenotypic characteristics of offspring during the postnatal period. The results indicated that pregnancy outcomes and postnatal development of NOS3-/- mice seem to be related to deficiencies in fetal programming mainly determined by maternal genotype. © 2010 by the Society for Biology of Reproduction.
| Main Authors: | , |
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| Format: | artículo biblioteca |
| Language: | English |
| Published: |
Elsevier
2010
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| Subjects: | Perinatal death, Postnatal development, Knockout mice, Nitric oxide, Pregnancy, |
| Online Access: | http://hdl.handle.net/20.500.12792/3303 http://hdl.handle.net/10261/292262 |
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| Summary: | Mice deficient for endothelial nitric oxide synthase (NOS3-/-) may represent a good model for studying embryo loss and intrauterine growth retardation caused by vascular deficiencies. We determined the effects of embryo genotype (homozygous vs. heterozygous descendants with paternal or maternal source of the non-functional NOS3 allele) and maternal environment (NOS3-/- vs. wild-type NOS3+/+ females) on the appearance of estrus, fertility and prolificacy rates and live weight in the first week of life as well as phenotypic characteristics of offspring during the postnatal period. The results indicated that pregnancy outcomes and postnatal development of NOS3-/- mice seem to be related to deficiencies in fetal programming mainly determined by maternal genotype. © 2010 by the Society for Biology of Reproduction. |
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