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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: The pathogenic role of succinate-SUCNR1: a critical function that induces renal fibrosis via M2 macrophage

Fig. 5

SUCNR1 was required for the effects of succinate on M2 polarization, upregulation of profibrotic factors, and paracrine actions on fibroblasts. RAW 264.7 was transfected with SUCNR1 siRNA for 36 h, and 500 μM succinate was stimulated for 24 h. A SUCNR1 mRNA levels were significantly reduced by SUCNR1 siRNA. &&&P < 0.001, versus succinate group, n = 3, biologically repeated 3 times. B Knockdown of SUCNR1 inhibited the downregulation of proinflammatory M1 cytokines (iNOS and IL6) and upregulation of anti-inflammatory M2 cytokines (Arg1, Fizz1, Mgl2, IL10) (C) induced by succinate. ***P < 0.001, versus the control group, &&&P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times. D The elevated profibrotic factors were also restored by SUCNR1 siRNA. ***P < 0.001, versus the control group, &&&P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times. E The proliferative effects of the conditioned medium in the succinate group were abolished by SUCNR1 siRNA. ***P < 0.001, versus the control group, &&&P < 0.001, versus the succinate group, n = 6, biologically repeated 3 times. F The enhanced protein expressions of fibronectin and α-SMA were reduced by SUCNR1 siRNA. ***P < 0.001, versus the control group, &&&P < 0.001, versus the succinate group, n = 3, biologically repeated 3 times

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