Depletion of SENP1-mediated PPARγ SUMOylation exaggerates intermittent hypoxia-induced cognitive decline by aggravating microglia-mediated neuroinflammation
Hongwei Wang, Wei Xiong, Sitong Hang, Yanmin Wang, Sisen Zhang, Song Liu
Abstract
. The Morris Water Maze results showed that both IH groups mice exhibited longer latency and shorter dwell-time in the goal quadrant than normoxia groups. Notably, SENP1 downregulation aggravated these alterations. Overall, these results showed that SENP1 played an essential role in IH-associated cognitive dysfunction. SENP1 depletion aggravated neuroinflammation and neuronal apoptosis via promoting the SUMOylation of PPARγ, reducing the level of PPARγ, thus exaggerating IH-induced cognitive decline.
Topics & Concepts
NeuroinflammationMicrogliaSUMO proteinDownregulation and upregulationCognitive declineInflammationHypoxia (environmental)Intermittent hypoxiaMorris water navigation taskApoptosisEndocrinologyInternal medicineChemistryBiologyMedicineHippocampusBiochemistryDementiaGeneUbiquitinObstructive sleep apneaOrganic chemistryOxygenDiseaseNeuroinflammation and Neurodegeneration MechanismsPeroxisome Proliferator-Activated ReceptorsImmune cells in cancer