Fig 2: Small interfering-RXR reverses the effects of miR-146a-5p on inflammation and ABCG1 in an in vitro model of refractory Mycoplasma pneu- moniae pneumonia. (A-D) Densitometry analysis of RXR, LXR, p65 and ABCG1 protein expression following western blotting. (E) Western blot gel. (F) TNF-α, (G) IL-1β, (H) IL-6, (I) IL-18, (J) COX-2 and (K) iNOS levels. **P<0.01 vs. negative group; ##P<0.01 vs. anti-146a-5p group. ABCG1, ATP-binding cassette subfamily G member 1; COX-2, cyclooxygenase-2; IL, interleukin; iNOS, inducible nitric oxide synthase; miR, microRNA; IRAK-1, interleukin 1 receptor-associated kinase 1; LXR, liver X receptor; RXR, retinoid X receptor; negative, negative mimics group; anti-146a-5p, downregulation of miR-146a-5p expression group; TNF-α, tumor necrosis factor-α.

Fig 3: Si-IRAK-1 reverses the effects of anti-miR-146a-5p on inflammation and ABCG1 in an in vitro model of refractory Mycoplasma pneumoniae pneumonia. (A-E) Densitometry analysis of IRAK-1, RXR, LXR, p65 and ABCG1 protein expression following western blotting. (F) Western blot gel. (G) TNF-a, (H) IL-1ß, (I) IL-6, (J) IL-18, (K) COX-2 and (L) iNOS levels. **P<0.01 vs. negative group; ##P<0.01 vs. anti-146a-5p group. ABCG1, ATP-binding cassette subfamily G member 1; COX-2, cyclooxygenase-2; IL, interleukin; iNOS, inducible nitric oxide synthase; IRAK-1, interleukin 1 receptor-associated kinase 1; LXR, liver X receptor; RXR, retinoid X receptor; negative, negative mimics group; anti-146a-5p, downregulation of microRNA-146a-5p expression group; Si, small interfering RNA; TNF-a, tumor necrosis factor-a.

Fig 4: MicroRNA-146a-5p regulates ABCG1/IRAK-1 protein expression in an in vitro model of refractory Mycoplasma pneumoniae pneumonia. (A-E) Densitometry analysis IRAK-1, RXR, LXR, p65 and ABCG1 protein expression following western blotting. (F) Western blot gel. **P<0.01 vs. negative group. ABCG1, ATP-binding cassette subfamily G member 1; IRAK-1, interleukin 1 receptor-associated kinase 1; LXR, liver X receptor; RXR, retinoid X receptor; negative, negative mimics group; anti-146a-5p, downregulation of microRNA-146a-5p expression group.

Fig 5: ATP7A mediated the miR-495-induced inhibition of angiogenesis in esophageal cancer cells. (A) Recovery of the angiogenic capabilities of HUVECs cocultured with cisplatin-resistant esophageal cancer cells overexpressing miR-495 as result of ATP7A overexpression. HUVEC angiogenesis was evaluated by the tube formation assay. (B,C) Levels of angiogenic factors in the culture media of cisplatin-resistant Eca-109 and TE1 cells overexpressing miR-495 and the ATP7A gene. ELISA methods were used to analyze the TNF-α (B) and VEGF (C) levels in cell culture media. (D) The levels of MRP1, ABCG1, ABCA1, VEGF, and C-Cas3 proteins in cisplatin-resistant esophageal cancer cells as altered by miR-495 and ATP7A overexpression. (E) The recovered expression of NLRP3 protein in cisplatin-resistant esophageal cancer cells transfected with miR-495 mimics and overexpressing ATP7A. NLRP3 protein expression in esophageal cancer cells was measured by immunofluorescence. Abbreviations: NC, negative control; ATP7A, ATPase copper transporting alpha; DDP, cisplatin; TNF-α, tumor necrosis factor alpha; VEGF, vascular endothelial growth factor; MRP1, multidrug resistance protein 1; ABCG1, ATP-binding cassette transporter-G1; ABCA1, ATP-binding Cassette Transporter A1; C-Cas 3, cleaved Caspase-3; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; NLRP3, NLR family, pyrin domain-containing 3; ELISA, enzyme linked immunosorbent assay; *P < .05; **P < .01.