Research Paper Volume 13, Issue 11 pp 15240—15254

Depletion of SENP1-mediated PPARγ SUMOylation exaggerates intermittent hypoxia-induced cognitive decline by aggravating microglia-mediated neuroinflammation


Figure 4. SENP1 depletion promotes the SUMOylation of peroxisome proliferator-activated receptor-γ (PPARγ) in mice under intermittent hypoxia (IH) condition. (A) The genotype of mice was identified by agarose gel electrophoresis. (B, C) The expression of SENP1 and SUMO-1 in mice with or without SENP1 knockdown under normoxic and IH conditions. ***p < 0.001 versus the normoxia groups; ###p < 0.001 versus the SENP1+/+-IH group. (DF) The effects of IH on the SUMOylation of PPARγ (D, E) and the level of PPARγ (D, F) were detected by co-immunoprecipitation followed by western blot analysis. ***p < 0.001 versus the normoxia groups. ##p < 0.01, ###p < 0.001 versus the SENP1+/+-IH group. Normoxia: mice were treated under normoxic condition. IH: mice were exposed under IH. SENP1+/+, wild type mice; SENP1+/−, SENP1 knockdown mice.