Fig. 3 | International Journal of Oral Science

Fig. 3

From: Oral pathogen aggravates atherosclerosis by inducing smooth muscle cell apoptosis and repressing macrophage efferocytosis

Fig. 3The alternative text for this image may have been generated using AI.

Inhibition of TLR2 signaling alleviates P. gingivalis-induced SMCs apoptosis and reduces miR-143/145 expression. a Influence of different concentrations of P. gingivalis on TLR-2 signaling (MYD88, Trif, and IRAK-4 protein expression), apoptosis-related markers (PARP, cleaved PARP, and Cleaved caspase3 protein expression), and NF-κB pathway (p-P65, P65, and Ikb-α in cytoplasmic extracts, and P65 in nuclear extracts). b Influence of inhibiting TLR2 signaling on apoptosis-related markers and NF-κB pathway. c Flow cytometry analysis for apoptotic SMCs with the stimulation of P. gingivalis and C29 (a TLR2 Inhibitor). d Relative miR-143/145 expression in the nucleus, cytoplasm, and apoEVs were measured by qRT-PCR when Pg-infected SMCs were treated with C29. e Immunostaining staining of α-SMA and Cleaved caspase3 in atherosclerotic lesions from TLR2+/+ApoE−/− or TLR2−/−ApoE−/− mice with P. gingivalis exposure or not. The yellow dotted line indicates the boundary between tunica intima and media. n = 6. Scale bars: 50 μm. f FISH staining showing the miR-143 (white arrowhead) and miR-145 (yellow arrowhead) expression in atherosclerotic plaque of TLR2+/+ApoE−/− or TLR2−/−ApoE−/− mice with P. gingivalis exposure or not. n = 6. Scale bars: 20 μm. The right panel shows the quantitative data. Results are presented as the mean ± S.D by one-way ANOVA followed by Tukey multiple comparisons tests. *P< 0.05; **P< 0.01; #P > 0.05

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