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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Circulating mitochondria promoted endothelial cGAS-derived neuroinflammation in subfornical organ to aggravate sympathetic overdrive in heart failure mice

Fig. 5

C-MitoHF highly expressed DHODH, which interacts with cGAS to facilitate brain endothelial cGAS activation. A Immunoblotting was conducted to detect DHODH expression in C-MitoCtrl and C-MitoHF. B The results of immunoblotting showed that the expression of DHODH was higher in C-MitoHF compared to C-MitoCtrl. t test. C Co-localization of DHODH and cGAS was detected by double-immunofluorescent staining in bEnd.3 cells. Scale bar = 10 μm. D The direct interaction between DHODH and cGAS was detected by co-immunoprecipitation. E, F Immunuoblotting results showed that C-MitoHF significantly increased endothelial cGAS expression, while teriflunomide pre-treatment on C-MitoHF significantly mitigated the cGAS-inducing effect of C-MitoHF in bEnd.3 cells. G Teriflunomide pre-treatment on C-MitoHF significantly mitigated the cGAMP-producing effect of C-MitoHF in bEnd.3 cells. H Pre-treated with Teriflunomide on C-MitoHF ameliorated the pro-inflammatory effect of C-MitoHF in bEnd.3 cells. n = 6, P < 0.05, ANOVA LSD test

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