Hsa-miR-346 plays a role in the development of sepsis by downregulating SMAD3 expression and is negatively regulated by lncRNA MALAT1.

Sepsis is a common complication in infection, trauma, and surgery. Severe sepsis has been identified as the leading cause of death in patients suffering from noncardiovascular ailments in intensive care units. In the current study, we used lipopolysaccharide (LPS) to stimulate the mouse macrophage cell line RAW264.7, and investigated the effects of the lncRNA MALAT1/hsa-miR-346/SMAD3 regulatory network on the progression of sepsis. We showed that MALAT1 inhibited RAW264.7 cell proliferation, while hsa-miR-346 promoted its proliferation. In this RAW264.7 cell model, MALAT1 inhibited hsa-miR-346 expression, and upregulated SMAD3 protein expression. The SMAD3 protein expression in RAW264.7 cells was significantly downregulated upon the overexpression of hsa-miR-346. These results suggest that the MALAT1/hsa-miR-346/SMAD3 regulatory network plays a key role in the development of sepsis, and may serve as a target for the treatment of sepsis.

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