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. 2021 Jan 20;14:265–277. doi: 10.2147/DMSO.S280765

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© 2021 Wang et al.

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EPB41L4A-AS1 knockdown induced MYD88-mediated activation of the NF-κB pathway. (A) Expression of phospho-p65 and p65 in shnc, shEPB41L4A-AS1-1, and shEPB41L4A-AS1-2 cells without LPS treatment and with 200 ng/mL LPS treatment. (B) Immunofluorescence localization of phospho-p65 in shnc, shEPB41L4A-AS1-1, and shEPB41L4A-AS1-2 cells after 200 ng/mL LPS treatment. Bar represents 20 μm. (C) MYD88 expression in PBMC expression microarray (GDS3874) for T2DM patients. (D) MYD88 expression in expression microarray of human PBMC treated with LPS (GDS2856). (E–F) mRNA and protein expression of MYD88 in shnc, shEPB41L4A-AS1-1, and shEPB41L4A-AS1-2 cells after 200 ng/mL LPS treatment. (G–I) mRNA expression of MYD88, IL-1B, and IL-8 in shEPB41L4A-AS1-sinc and shEPB41L4A-AS1-siMYD88 cells after 200 ng/mL LPS treatment. (J) Expression of phospho-p65 and p65 in shEPB41L4A-AS1-sinc and shEPB41L4A-AS1-siMYD88 cells without LPS treatment and with 200 ng/mL LPS treatment. Data are shown as mean ± SD. *P<0.05, **P<0.01, ***P<0.001; Student’s t-test.