Modulation of oligosaccharyltransferase isoforms expression at early mouse pregnancy

M. B, PRADOS; S. MIRANDA

Georgia

Congreso; Second World Congress of Glycobiology; 2016

OMICS International

Title: Modulation of oligosaccharyltransferase isoforms expression at early mouse pregnancyName: María B. Prados1-2 and Silvia E. Miranda11ININCA (CONICET-UBA). Buenos Aires. ARGENTINA2 Present address: Centro Atómico Bariloche, Av. Bustillo 9500, S.C. Bariloche, Rio Negro, ArgentinaThe oligosaccharyltransferase (OST) catalyzes the N-glycosylation of polypeptides entering the endoplasmic reticulum (ER) in eukaryotic cells. Two isoforms of its catalytic subunit (STT3-A and STT3-B) can assemble in OST complexes, providing different turnover rates and specificity. We reported previously that progesterone modulated the expression of STT3-A and STT3-B proteins in vitro, and modified the N-glycosylation pattern of a secreted IgG. In the present work, we analysed the expression of STT3 isoforms in implantation sites from a high fetal loss mouse model (CBA/J females mated with DBA/2J males) and a low fetal loss one (CBA/J females mated with BALB/c males). We also studied the influence of sound stress suffered early in gestation, on the proteins? expression. This stress diminishes progesterone circulating levels in the high fetal loss combination, as reported earlier. To this aim, DBA/2J and BALB/c mated CBA/J female mice were randomized in control and stressed groups (n=10) and sacrificed on gestation day 6.5. Implantation sites were removed and cryo-sectioned. The expression of STT3-A and STT3-B was investigated by immunohistochemistry. Results showed that STT3-A was expressed on decidual glands and on the uterine epithelial lining in both models, while STT3-B was expressed only in the vascular endothelium of the high fetal loss combination. Interestingly, sound stress altered the STT3-A/STT3-B ratio in the epithelium lining of both models: it diminished STT3-A expression in the high fetal loss model only but it upregulated STT3-B in both mouse models. In conclusion, this work demonstrates that the expression of OST isoforms can be regulated during pregnancy and by a pathological stimuli such as stress. Results suggest that progesterone could mediate these effects.