Stress increases VCAM-1 expression at the fetomaternal interface in an abortion prone mouse model.

PRADOS MB; SOLANO ME; FRIEBE A; BLOIS S; ARCK P; MIRANDA S

Congreso; 1º Congreso Franco Argentino de Inmunología; 2010

Numerous mechanisms involved in abortion processes have been described locally at the fetomaternal interface and systemically, largely arising from studies employing the high fetal loss mouse model (CBA/JxDBA/2J, H-2KxH-2d). A 24hs sound stress at 5.5 gestation day (gd) increased the fetal resorption rate (FRR) of DBA/2J mated CBA/J mice but not of BALB/C mated CBA/J females (low fetal loss model, H-2KxH-2d). Sound stress increases fetal loss via inflammatory pathways. Inflammation up-regulates cell adhesion molecules, which induce cell recruitment to the site of inflammation. In this context, vascular cell adhesion molecule-1 (VCAM-1) mediates the adhesion of leukocytes to vascular endothelium after the endothelial cells have been stimulated by cytokines like TNF- Thus, we aimed to study the frequency of VCAM-1+ vessels at fetomaternal interface in stressed and non-stressed pregnant CBA/J female mice mated with DBA/2J or BALB/C males. Pregnant females were divided into control and stressed groups. The latter were exposed to sound stress at gd 5.5 during 24hs. Both groups were sacrificed on gd 6.5, implantation units were removed and cryo-sectioned. The number of vessels per tissue section was determined by PECAM immunostaining. Vessels were classified into small, medium and large according to its size. VCAM-1 expression was analyzed by immunohistochemistry in the cryosections. We observed that both stressed groups had similar number of large vessels. However, stress duplicated the number of large vessels expressing VCAM-1 in the high fetal loss model (p