MiR-29b aggravates lipopolysaccharide-induced endothelial cells inflammatory damage by regulation of NF-κB and JNK signaling pathways

MicroRNAs (miRNAs) have been reported to involve in variety of biological progresses. The present study aimed to explore the functional roles of miR-29b in endothelial cells inflammatory damage, as well as the underlying mechanisms. Lipopolysaccharide (LPS) was used to induce endothelial cell inflammation, and the role of miR-29b in endothelial cells inflammatory damage was detected by testing cell viability, cell apoptosis, and the expression of inflammation factors after the suppression or overexpression of miR-29b. Aiming to make clear of the underlying mechanism of miR-29b regulation in inflammation, we studied the relationship between miR-29b and NF-κB/JNK pathway in HUVEC and Eahy926 cells. The results showed that LPS significantly suppressed cell viability, promoted apoptosis and increased TNF-α, IL-1α and INF-γ secretions. MiR-29b was up-regulated in LPS-treated HUVEC and Eahy926 cells. Moreover, suppression of miR-29b alleviated LPS-induced inflammatory injury by promoting cell viability, decreasing apoptosis and reducing the secretions of TNF-α, IL-1α and INF-γ in both HUVEC and Eahy926 cells. On the contrary, overexpression of miR-29b aggravated cell inflammatory injury in both HUVEC and Eahy926 cells. Furthermore, LPS activated NF-κB and JNK signal pathways. However, suppression of miR-29b reduced LPS-activated NF-κB and JNK pathways in both HUVEC and Eahy926 cells. Taken together, these findings concluded that miR-29b could regulate LPS-induced endothelial cells inflammatory injury through regulation of NF-κB and JNK signaling pathways.