Modulation of oligosaccharyltransferase isoforms expression at early mouse pregnancy

M. BELÉN PRADOS; SILVIA MIRANDA

Atlanta

Congreso; 2nd Glycobiology World Congress; 2016

p { margin-bottom: 0.25cm; direction: ltr; color: rgb(0, 0, 10); line-height: 120%; text-align: left; }p.western { font-family: "Times New Roman",serif; font-size: 12pt; }p.cjk { font-family: "Batang"; font-size: 12pt; }p.ctl { font-family: "Times New Roman"; font-size: 12pt; }Theoligosaccharyltransferase (OST) catalyzes the N-glycosylation ofpolypeptides entering the endoplasmic reticulum (ER) in eukaryoticcells. Two isoforms of its catalytic subunit (STT3-A and STT3-B) canassemble in OST complexes, providing different turnover rates andspecificity. We reported previously that progesterone modulated theexpression of STT3-A and STT3-B proteins in vitro, and modified theN-glycosylation pattern of a secreted IgG. In the present work, weanalysed the expression of STT3 isoforms in implantation sites froma 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). Wealso studied the influence of sound stress, suffered early ingestation, in the protein's expression. This stress diminishesprogesterone circulating levels in the high fetal loss combination,as reported earlier. To this aim, DBA/2J and BALB/c mated CBA/Jfemale mice were randomized in control and stressed groups (n=10) andsacrificed on gestation day 6.5. Implantation sites were removed andcryo-sectioned. The expression of STT3-A and STT3-B was investigatedby immunohistochemistry. Results showed that STT3-A was expressed ondecidual glands and on the uterine epithelial lining in both models,while STT3-B was expressed only in the vascular endothelium of thehigh fetal loss combination. Interestingly, sound stress altered theSTT3-A/STT3-B ratio in the epithelium lining of both models: itdiminished STT3-A expression in the high fetal loss model only but itupregulated STT3-B in both mouse models. In conclusion, this workdemonstrates that the expression of OST isoforms can be regulatedduring pregnancy and by a pathological stimuli such as stress.Results suggest that progesterone could mediate these effects.