We aim to investigate whether microRNA-106b (miR-106b) affects the inflammation injury of cardiac endothelial cells (ECs) by targeting B-cell linker (BLNK) via the NF-êB signaling pathway. Human cardiac microvascular endothelial cells (HCMECs) were assigned into the control, hypoxia/reoxygenation (H/R), negative control (NC), pyrrolidine dithiocarbamate (PDTC), miR-106b mimic, miR-106b inhibitor, and si-BLNK, and miR-106b inhibitor+si-BLNK groups. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting were conducted for miR-106b expression and expressions of BLNK, interleukin (IL)-6, IL-1â, tumor necrosis factor (TNF)-á, NF-êB, pIêBá, BTK, and PLC-ã2. Enzyme-linked immunosorbent assay was applied for levels of IL-6, IL-10, and TNF-á; cell counting Kit-8 assay for cell proliferation; and flow cytometry for cell cycle and ensuing apoptosis. In-vitro tube formation assay was performed for tube formation ability. Dual-luciferase reporter assay revealed that BLNK was verified as the target gene of miR-106b. Compared with the H/R and NC groups, the PDTC, miR-106b mimic, and si-BLNK groups had declined expressions of IL-6, IL-1â, TNF-á, BTK, PLC-ã2, NF-êB p105/p50, and pIêBá as well as levels of L-6 and TNF-á, but contrarily elevated levels of NF-êB p105/p50 and IL-10. The PDTC, miR-106b mimic, and si-BLNK groups had less cell number in G0 /G1 phase but higher cell count in both S and G2 phases, decreased cell apoptosis but increased proliferation and tube formation ability, while opposite trends were observed in the miR-106b inhibitor group. Our findings indicated that the overexpression of miR-106b alleviated the inflammation injury of cardiac ECs by targeting BLNK via the NF-êB signaling pathway.
Adaptor Proteins, Signal Transducing Apoptosis