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. Author manuscript; available in PMC: 2016 Dec 15.
Published in final edited form as: Toxicol Appl Pharmacol. 2015 Oct 28;289(3):457–465. doi: 10.1016/j.taap.2015.10.015

Figure 6. Effects of JMJD2B knockdown on PCB-induced vascular inflammation.

Figure 6

(A) JMJD2B knockdown was validated at mRNA and protein levels. Whole-cell lysates from endothelial cells were immunoblotted with antibodies against JMJD2B after 24 h treatment of siRNAs. NF-κB subunit p65 expression was also examined. GAPDH is the loading control. (B) Knockdown of JMJD2B led to significant reduction of PCB-induced p65 and IL-6 expression, measured by qRT-PCR. (C) JMJD2B knockdown reduced the accumulation of JMJD2B in the p65 promoter induced by PCB exposure. (D) JMJD2B knockdown abolished PCB-induced removal of H3K9me3 repression mark in the p65 promoter. *Significantly increased compared to the DMSO control. #Significantly decreased compared to the siRNA control group. siC, siControl; siJ, siJMJD2B; D, DMSO; 77, PCB 77; 126, PCB 126.