Skip to main content
. 2016 Mar 28;18(10):1379–1389. doi: 10.1093/neuonc/now049

Fig. 5.

Fig. 5.

PGE2 signaling regulates radiation resistance in mouse glioblastoma (GBM) primary cultures in an Id1-dependent manner. (A) Treatment of mouse Id1+/+, Id3+/+ GBM cultures with 10 Gy ionizing radiation (IR) induced significant cleavage of caspase-3 after 4 hours. This increase was attenuated by pretreatment with 0.5 µM dmPGE2. Scale bar = 0.01 mm. (B) Quantification of immunostaining from (A). Error bars represent mean ± SEM (n = 3). *, P < .05. C, Id1 −/− , Id3 +/− GBM cultures were treated as described in panel A. In comparison with the Id1+/+, Id3+/+ cells, the radioprotective effects of dmPGE2 were blunted. Scale bar = 0.2 mm. (D) Quantification of immunostaining from (C). Error bars represent mean ± SEM (n = 3). *, P < .05. (E) Treatment of mouse Id1+/+, Id3+/+ GBM cultures with 0.5 µM dmPGE2 for 24 hours was associated with decreased Parp1 cleavage. This protective effect was not observed in Id1 −/− , Id3 +/− GBM cells. F, Pretreatment with 5 µM celecoxib for 24 hours increased Parp1 cleavage in Id1/3 wild type cells, but not in Id1 −/− , Id3 +/− cells.