Fetal and maternal transforming growth factor-beta 1 may combine to maintain pregnancy in mice.
Biol Reprod
; 70(6): 1614-8, 2004 Jun.
Article
en En
| MEDLINE
| ID: mdl-14766723
ABSTRACT
One of the mysteries of pregnancy is why a mother does not reject her fetuses. Cytokine-modulation of maternal-fetal interactions is likely to be important. However, mice deficient in transforming growth factor-beta1 (TGF beta 1) and other cytokines are able to breed, bringing this hypothesis into question. The phenotype of TGF beta 1 null-mutant mice varies with genetic background. We report here that, in outbred mice, the loss of TGF beta 1-deficient embryos is influenced by the parity of their mother. This is consistent with the loss of mutants being due to immune rejection. An inbred line of TGF beta 1(+/-) mice that supported TGF beta 1-deficient fetuses had high levels of TGF beta 1 in their plasma. Analysis of the amniotic fluids in this line indicated that biologically relevant levels of maternal TGF beta 1 were present in the TGF beta 1(-/-) fetuses. These data are consistent with maternal and fetal TGF beta 1 interacting to maintain pregnancy, within immune-competent mothers.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Factor de Crecimiento Transformador beta
/
Intercambio Materno-Fetal
Límite:
Animals
/
Pregnancy
Idioma:
En
Revista:
Biol Reprod
Año:
2004
Tipo del documento:
Article
País de afiliación:
Nueva Zelanda