Title : The role of GLS1-mediated glutaminolysis/2-HG/H3K4me3 and GSH/ROS signals in Th17 responses counteracted by PPARγ agonists.

Pub. Date : 2021

PMID : 33754076






3 Functional Relationships(s)
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1 Results: The PPARgamma agonists rosiglitazone and pioglitazone blocked glutaminolysis but not glycolysis under Th17-skewing conditions, as indicated by the detection of intracellular lactate and alpha-KG and the fluorescence ratios of BCECF-AM. Rosiglitazone peroxisome proliferator activated receptor gamma Mus musculus
2 However, the limitation of PPARgamma agonists on the mRNA expression of RORgammat was unable to be stopped by 2-HG but was attributed to GSH/ROS signals subsequent to GLS1. Rosiglitazone peroxisome proliferator activated receptor gamma Mus musculus
3 Conclusion: PPARgamma agonists repressed Th17 responses by counteracting GLS1-mediated glutaminolysis/2-HG/H3K4me3 and GSH/ROS signals, which is beneficial for Th17 cell-related immune dysregulation. Rosiglitazone peroxisome proliferator activated receptor gamma Mus musculus