Sound stress induces a switch in the expression of oligossacariltranferase isoforms at maternofetal interface in an abortion prone mouse model

PRADOS MB; SOLANO ME; FRIEBE A; LOPEZ MEDUS M; CARAMELO J; ARCK P; MIRANDA S

CABA

Congreso; First French-Argentine Immunology Congress; 2010

SAI-Grupo Rioplatense de Citometría-SAP (Inmunología pediátrica)

A 24hs sound stress at gestation day (gd) 5.5 increases the abortion rate of DBA/2J mated CBA/J mice (high fetal loss mouse model) but not of BALB/C mated CBA/J females (low fetal loss model). This fetal loss is accompanied by a decreased in protective extra-N-glycosylated antibodies and progesterone (P4) levels in serum. Oligosaccharyltransferase (OST) is responsible for the N-glycosylation of proteins. We previously demonstrated that P4 modulates OST catalytic subunit expression (STT3-A or STT3-B) in a murine hybridoma with consequences on IgG N-glycosylation. In order to investigate an in vivo modulation of OST isoform expression, we analyzed STT3-A and B expression at maternofetal interface in non-stressed and stressed pregnant CBA/J female mice mated with DBA/2J or BALB/C males. Sound stress (300 Hz in intervals of 15s) was applied at gd 5.5 during 24hs. All mice were sacrificed on gd 6.5 and implantation units were removed and cryosectioned. STT3-A and B expression was analyzed by immunohistochemistry and scored from 0 to 4. STT3-A and B reactivity localized preferentially in glands (G), vessels (V) and lumenal epithelium (LE) but with different expression levels of each isoform in each group. In BALB/C mating: the highest STT3-A expression was found in G (3.8±0.5) and LE (2.8±0.5) while V staining was weak (0.3±0.3). In contrast, STT3-B expression was similar in all the structures (G: 0.7±1.2, LE: 1.0±0.1 and V: 0.5±0.5). In DBA/2J mating, similar results were observed for STT3-A expression (G: 3.8± 0.5; LE: 3.3±0.9 and V: 1.3±0.5). However, STT3-B expression was higher in V than in the other structures (G: 1.8±0.9, LE: 1.3±05 and V: 3.3±0.5) in this model. Stress increased STT3-B expression (2.3 folds) in the LE of BALB/C and DBA/2J mated females. However, in the case of DBA/2J mated females, stress also decreased STT3-A (0,43 folds). We did not observe any differences in the rest of the tissue. In conclusion, stress differentially modulates the expression of STT3-A and B in the low and in the high fetal loss model. The physiological relevance of this observation is being addressed.