Inflammatory Factors Induce Thrombosis through the miR-146b-3pp38MAPKCOX-2 Pathway

Abstract EN

Objective.

Inflammatory responses play important roles in the pathogenesis of atherosclerosis.

The purpose of this study was to investigate the relationship between microRNA-146b-3p (miR-146b-3p) and inflammatory factors in thrombosis.

Method.

THP-1 cells were cultured in vitro, Western blot was used to determine the protein levels of COX-2 and p38MAPK in the cells, and real-time PCR was used to detect the mRNA expression of miRNA-146b-3p and COX-2.

A lentiviral expression vector of miRNA-146b-3p and its inhibitor were constructed to transfect THP-1 cells.

COX-2 and p38MAPK expression in transfected cells was detected by Western blot and real-time PCR, respectively.

Results.

Ang II and TNF-α could elevate the expression of COX-2 in monocytes.

The expression of COX-2 was upregulated by p38MAPK, which could be phosphorylated by Ang II, while there was an increasing tendency of p38MAPK phosphorylation after TNF-α stimulation.

In addition, COX-2 expression and P38MAPK phosphorylation could be downregulated by miRNA-146b-3p and upregulated by the miRNA-146b-3p inhibitor.

Ang II could increase miR-146b-3p expression, although there was no significant difference; however, the expression of miR-146b-3p was enhanced significantly by TNF-α.

Conclusion.

Our data implied that altered expression of miR-146b-3p was closely related to the progression of inflammation mediating the P38MAPK/COX-2 pathway.

We suggest that the miR-146b-3p/p38MAPK/COX-2 pathway plays a key role in inflammation and arterial thrombosis.