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. 2021 Feb 18;12:633353. doi: 10.3389/fphar.2021.633353

FIGURE 4.

FIGURE 4

miR-511-3p is involved in periodontitis by modulating TLR4, and silencing circMAP3K11 (si-circMAP3K11) reverses the effect of miR-511-3p inhibitor on TLR4 expression in PDLSCs (A) The putative complementary binding sites within TLR4 and miR-511-3p predicted by TargetScan (B) The binding sites of miR-511-3p in the 3′UTR of TLR4, and the mutated version of the TLR4 3′UTR is also shown (C) The dual-luciferase reporter assay was performed to confirm that TLR4 is a direct target gene of miR-511-3p (D) Immunohistochemistry observed the protein expression level of TLR4 in periodontitis and normal samples (E) The expression level of TLR4 in periodontitis and normal samples was detected by RT-PCR (F) Spearman’s correlation analysis showed a negative correlation between TLR4 and miR-511-3p expression in periodontitis samples (G) RT-PCR examined the expression of TLR4 in PDLSCs transfected with miR-511-3p mimic or corresponding control (H) The promotion on cell viability in PDLSCs by TLR4 overexpression was attenuated by miR-511-3p mimic (I) si-circMAP3K11 reverses the effect of miR-511-3p inhibitor on TLR4 expression in PDLSCs. Note: *p < 0.05, **p < 0.01, and ***p < 0.005, vs. control; #p < 0.05, ##p < 0.01, and ###p < 0.005, vs. TLR4 OE or si-circMAP3K11.