CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
CELL PROLIFERATION AND DEATH IN PLACENTA ASSOCIATED WITH FETAL GROWTH RESTRICTION
Autor/es:
MARINO ANACLARA; WOLFSON MANUEL LUIS; SCHANDER JULIETA AYLEN; AISEMBERG, JULIETA; CAROLINA MARVALDI; FRANCHI ANA MARÍA
Reunión:
Congreso; 53rd SSR Annual Meeting (SRI); 2020
Institución organizadora:
SRI
Resumen:
Intrauterine growth restriction (IUGR) is a condition whereby a fetus isunable to achieve its genetically determined potential size. Prenatal stress isone of the causes that alter the intrauterine environment, which affects thenormal development and function of the placenta, and the fetal growth. Furthermore,IUGR is associated with placental dysfunction, where altered trophoblast cellsturnover and function contribute to reduced feto-placental growth. The balance betweenplacental cell proliferation and death is a key point during the development ofthe fetus.The aim of this work was to study the differences in cell proliferation,apoptosis and autophagy in placental tissue in normal and IUGR placentas. The IUGRmouse model used was animals treated with a synthetic glucocorticoid duringlate pregnancy to cause growth restriction.Pregnant BALB/c mice received 8 mg/kg (s.c.) of dexamethasone betweendays 14 and 15 of pregnancy. The control group was sham-treated with saline.Prenatal glucocorticoid treatment not only induced fetal growth restriction butalso decreased placental weight. Placental tissue from pregnant animals wasdissected on gestational days 15 to 18 and processed for Western Blot andRT-qPCR analysis. The results were analyzed with a one-way ANOVA and Tukey test(p<0,05).Mice with IUGR presented higher placental levels of mRNA of PCNA on day16 and lower Bcl2 protein levels on day 15 (p˂0,05) compared with control groups. In addition, regardingcell proliferation, there were lower mRNA levels of Cyclin B1 and p57 cellcycle inhibitor on day 16. We found higher protein levels of LC3B-II(p˂0,05) on day 18 placentas compared with controls groups. There were nosignificant changes in mTOR, Bax, Fas and Fas ligand, Cyclin D3 or in the p16cell cycle inhibitor between studied groups. Therefore, during the day 15 and16, the mechanism of cell proliferation and apoptosis were altered in IUGRplacentas. In term placentas the autophagy increases.In conclusion, IUGR induced by prenatal dexamethasone treatment produces alterations on placental markers expression associated to cellproliferation, cell death and autophagy.