Triiodothyronine Represses MUC5AC Expression by Antagonizing Sp1 Binding to Its Promoter in Human Bronchial Epithelial HBE16 Cells

Figure 3

T3 selectively antagonizes Sp1 but not NF-κB-dependent transcription of MUC5AC in HBE16 cells. (a) After the cells were cotransfected with Sp1 expression plasmid, the luciferase activity was determined as described in Materials and Methods. Blank: different MUC5AC promoter plasmids only; control: different MUC5AC promoter plasmids plus Sp1 expression plasmid in the absence of T3; experimental: different MUC5AC promoter plasmids plus Sp1 expression plasmid in the presence of T3. ^∗𝑃>0.05 versus blank; ^∗∗𝑃<0.01 versus blank; ^#𝑃>0.05 versus control; ^##𝑃<0.01 versus control. (b) After the cells were cotransfected with NF-κB expression plasmid, the luciferase activity was determined as described in Materials and Methods. Blank: different MUC5AC promoter plasmids only; control: different MUC5AC promoter plasmids plus NF-κB expression plasmid in the absence of T3; experimental: different MUC5AC promoter plasmids plus NF-κB expression plasmid in the presence of T3. ^∗𝑃>0.05 versus blank; ^∗∗𝑃<0.01 versus blank; ^#𝑃>0.05 versus control. (c) After the cells were cotransfected with Sp1 expression plasmid and MUC −324/+48 promoter plasmid or its mutation form (mut), the luciferase activity was determined as described in Materials and Methods. Control: in the absence of T3; experimental: in the presence of T3. *𝑃<0.01 versus −324/+48 control group; ^#𝑃>0.05 versus −324/+48 mut control group.

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