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. Author manuscript; available in PMC: 2022 Mar 18.
Published in final edited form as: Glia. 2020 Sep 14;69(2):424–435. doi: 10.1002/glia.23907

Figure 2: Deletion of Xbp1 potentiates ERSR toxicity in primary mOPCs.

Figure 2:

Plp-creERT2+/+:Xbp1fl/fl mice-derived mOPCs were pretreated with vehicle (Veh) or tamoxifen (Tx) to delete Xbp1 and then treated with tunicamycin (Tm) or thapsigargin (Tg) to induce ER stress. A, Total RNA was isolated after 8 hours (h) of Tm and Tg treatment and analyzed for Xbp1s, ERdj4 and Edem transcript levels as indicated. mRNA levels (normalized to Gapdh) were expressed as fold changes compared to levels in the respective control cells. B,C Xbp1 deletion enhanced ER stress-mediated decreases in viable mOPC number (as evaluated by MTT assay, B) and ER stress-induced cell death (as evaluated by LDH release, C) after 24 hours of Tm and Tg treatment. Data are the mean ± SD, (n = 4, **p<0.01, ***p<0.001; Tx vs. Veh).