In the pregnant mouse endometrium, collagen fibrillogenesis is characterized by the presence of very thick collagen fibrils which are topographically located exclusively within the decidualized stroma. This dynamic biological process is in part regulated by the small leucine-rich proteoglycans decorin and biglycan. In the present study we utilized wild-type (Dcn + ⁄ + ) and decorin-deficient (Dcn) time-pregnant mice to investigate the evolution of non-decidualized and decidualized collagen matrix in the uterine wall of these animals. Ultrastructural and morphometric analyses revealed that the organization of collagen fibrils in the pregnant endometrium of both nondecidualized and decidualized stroma showed a great variability of shape and size, regardless of the genotype. However, the decidualized endometrium from Dcn ) ⁄ ) mice contained fibrils with larger diameter and more irregular contours as compared to the wild-type littermates. In the Dcn ) ⁄ ) animals, the proportion of thin (10-50 nm) fibrils was also higher as compared to Dcn + ⁄ + animals. On day 7 of pregnancy, biglycan was similarly localized in the decidualized endometrium in both genotypes. Lumican immunostaining was intense both in decidualized and non-decidualized stroma from Dcn ) ⁄ ) animals. The present results support previous findings suggesting that decorin participates in uterine collagen fibrillogenesis. In addition, we suggest that the absence of decorin disturbs the process of lateral assembly of thin fibrils, resulting in very thick collagen fibrils with irregular profiles. Our data further suggest that decorin, biglycan and lumican might play an interactive role in collagen fibrillogenesis in the mouse endometrium, a process modulated according to the stage of pregnancy.

Um aumento no potencial hemostático endometrial ocorre durante o ciclo menstrual, possibilitando, assim, a implantação embrionária, caso ocorra a fertilização. Defeitos nas proteínas de coagulação podem alterar esse estado de hipercoagulabilidade gestacional e desencadear perdas fetais por falhas na implantação ou na nutrição do embrião. A síndrome do aborto recorrente pode ser ocasionada por inúmeros fatores, entre eles anormalidades cromossômicas, anatômicas ou hormonais, ou ainda por defeitos nas proteínas de coagulação sanguínea ou plaquetária. Uma causa comum de abortos recorrentes é a síndrome antifosfolípide, uma desordem sistêmica, autoimune, caracterizada por trombose arterial e/ou venosa, morte fetal, abortos recorrentes e trombocitopenia, acompanhada de títulos elevados de anticorpos antifosfolípides: anticoagulante lúpico e/ou anticardiolipina. Pela íntima associação dessas síndromes, faz-se necessário investigá-las em pacientes que procuram os tratamentos de fertilização in vitro. Palavras-chave: Síndrome antifosfolipídica; aborto habitual; inibidor de coagulação do lúpus; anticorpos anticardiolipina.

Título da Dissertação:Efeitos da duração do diabetes mellitus tipo 1 sobre ciclo estral, a placenta e o desenvolvimento fetal em camundongos.

Diabetes progression promoted distinct outcomes in pregnancy. Modifications of both synthesis and turnover of ECM occurred even before changes of placental weight were detected. Adjustment of fetal/placental weight ratio or placental enlargement restored normal growth in part of the fetuses from the long-term group.

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