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. Author manuscript; available in PMC: 2022 Feb 18.
Published in final edited form as: Glia. 2020 Sep 16;69(2):489–506. doi: 10.1002/glia.23910

Figure 10. PERK inactivation exacerbated SC loss in the PNS of adult Sel1L cKO mice.

Figure 10.

A-D, M, N. S100 and cleaved caspase-3 (CC3) double immunostaining showed that the number of SCs was significantly reduced in the sciatic nerve of 16-w-old Sel1L cKO mice compared to PERK cKO mice and control mice, and was further reduced in Double cKO mice. Importantly, the number of cleaved-caspase 3 positive SCs (arrow) was significantly increased in Sel1L cKO mice compared to PERK cKO mice and control mice, and was further increased in Double cKO mice. ND, undetectable. E-H, O, P. Krox-20 and c-Jun double immunostaining showed that the number of Krox-20 positive cells was significantly decreased in the sciatic nerve of 16-w-old Sel1L cKO mice compared to PERK cKO mice and control mice, and was further decreased in Double cKO mice. The number of c-Jun positive cells in the sciatic nerve of 16-w-old Sel1L cKO mice was significantly increased compared to PERK cKO mice and control mice, but was not significantly changed compared to Double cKO mice. Arrow, Krox-20 and c-Jun double positive cells; arrowhead, c-Jun positive cells. I-L, Q. EM analysis showed that neither Sel1L deficiency nor PERK inactivation alter the morphology of SCs or the morphology of the ER (insets) in SCs in the sciatic nerve of 16-w-old mice. Importantly, double deficiency of Sel1L and PERK led to significantly enlarged ER lumen (insets) in SCs in the sciatic nerve of 16-w-old mice. Scale bars: A-D, 50 μm; G-J, 1.0 μm. N = 4 animals. Statistical analyses were done with a 1-way ANOVA with a Tukeys posttest. Error bars represent SD, P < 0.05.