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. 2019 Apr;189(4):797–812. doi: 10.1016/j.ajpath.2018.12.016

Figure 5.

Figure 5

Role of transforming growth factor-β–activating kinase (TAK)-1 in the lipopolysaccharide (LPS)-induced activation of canonical NF-κB pathway and Caco-2 tight junction permeability. A: LPS treatment at the concentration of 300 pg/mL caused activation of phospho-TAK-1. B and C: LPS treatment did not induce phosphorylation of NF-κB–inducing kinase (NIK) or mitogen-activated kinase kinase (MEKK)-1 at day 3 after LPS exposure compared with untreated Caco-2 cells. D: Confocal immunofluorescence of Caco-2 cells treated with 300 pg/mL LPS for 5 days indicated increase in pTAK-1 (green) on day 3 and 3.5 after LPS treatment. Nucleus, blue. E: TAK-1, NIK, and MEKK-1 siRNA transfections in Caco-2 cells significantly reduced TAK-1, NIK, and MEKK-1 protein expression, as analyzed by Western blot analysis and relative densitometry, respectively. F: TAK-1 siRNA transfection prevented the LPS-induced drop in Caco-2 cell transepithelial electrical resistance (TER). G: TAK-1 siRNA transfection inhibited the LPS-induced increase in Caco-2 inulin flux. H: NIK or MEKK-1 siRNA in transfection in Caco-2 cells did not prevent the LPS-induced drop in Caco-2 TER. Data are expressed as means ± SEM. n = 4 experiments (A). ∗∗∗P < 0.001 versus control; ††P < 0.01 versus LPS day 3; ‡‡P < 0.01 versus LPS day 3.5; §§P < 0.01 versus nontarget (NT) siRNA. Scale bars = 5 μm. C, control.