Skip to main content
Fig. 4 | Journal of Translational Medicine

Fig. 4

From: GDF11 alleviates neointimal hyperplasia in a rat model of artery injury by regulating endothelial NLRP3 inflammasome activation and rapid re-endothelialization

Fig. 4

GDF11 inhibited NLRP3 inflammasome activation by reducing LOX-1 expression. A Casp1 mRNA levels were higher in injured rat carotid arteries than in normal arteries in cohorts derived from the GEO database (https://www.ncbi.nlm.nih.gov/gds/). B The LOX-1 mRNA levels were higher in injured rat carotid arteries than in normal arteries in cohorts derived from the GEO database. C There was a positive correlation between LOX-1 and Casp1 transcript levels in the enrolled samples from the GEO datasets. The samples were obtained from injured rat carotid arteries in the GSE164050 dataset. D, E The effect of GDF11 on the expression of LOX-1 in the human endothelial cells treated with lysoPC was analyzed by Western blotting. F–H Human endothelial cells were transfected with 50 nM si-LOX-1. At 48 h post-transfection, qPCR and Western blotting were used to detect LOX-1 knockout. I, J The effect of si-LOX-1 on the expression of NLRP3 inflammasome components (NLRP3, Casp1 p20, and IL-1β) and GSDMD-N in human endothelial cells treated with lysoPC was analyzed by Western blotting. & p < 0.05 vs. the normal arteries; * p < 0.05 vs. the control group; # p < 0.05 vs. the lysoPC group

Back to article page