Figure 3: Manipulation of CD36 expression regulates NF-κB and JNK activation but not the p38-MAPK kinase pathway in pGMECs exposed to LPS stimulation. | Scientific Reports

Figure 3: Manipulation of CD36 expression regulates NF-κB and JNK activation but not the p38-MAPK kinase pathway in pGMECs exposed to LPS stimulation.

From: CD36 regulates lipopolysaccharide-induced signaling pathways and mediates the internalization of Escherichia coli in cooperation with TLR4 in goat mammary gland epithelial cells

Figure 3

(A,B) The NF-κB-RE and Renilla luciferase vectors were cotransfected into pGMECs. Then, CD36 expression was manipulated followed by stimulation with LPS for 12 h, and the transcriptional activity of the NF-κB promoter was evaluated. (C) Overexpression or knockdown of CD36 expression on LPS-stimulated pGMECs influenced NF-κB p65 protein expression. (D,E) AP-1 luciferase activity was influenced by the CD36 expression status in LPS-stimulated cells. (F) c-Jun protein levels increased in Ad-CD36 cells and decreased in si-CD36 cells treated with LPS for 12 h. (G) p38-MAPK protein levels were detected in LPS-stimulated cells (Ad-CD36 or si-CD36). The corresponding mean gray values of NF-κB p65, c-Jun, and p38-MAPK protein levels were obtained from three separate blots. The graph shows the densitometric quantification of NF-κB p65/β-actin, c-Jun/β-actin, and p38-MAPK/β-actin as the fold change difference compared to the control. The relative mRNA levels of MyD88 were also detected. All data are presented as the mean ±SEM from three experiments. *P < 0.05, **P < 0.01, and not significant (NS).

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