PVT1 knockdown inhibited the biological behavior of LPS-induced cardiac fibroblasts by regulating miR-24.

BACKGROUND

The heart is one of the target organs vulnerable to sepsis. About 50% of sepsis patients will suffer from myocardial injury and cardiac dysfunction, which will aggravate the sepsis and affect its prognosis.

OBJECTIVES

Here, we attempt to investigate the function of long non coding RNA PVT1 in LPS-induced cardiac fibroblasts in vitro, and explore its potential mechanism.

METHODS

The expression of PVT1 in LPS-induced cardiac fibroblasts was detected by qRT-PCR. CCK-8 assay, cell migration, qRT-PCR and western blotting analysis were applied to evaluating the effect of PVT1 knockdown on LPS-induced cardiac fibroblasts. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism.

RESULTS

PVT1 expression was up-regulated in LPS-induced cardiac fibroblasts. And knockdown of PVT1 inhibited cell viability and migration, alleviated inflammation cytokines production of LPS-treated cardiac fibroblasts. The bioinformatics analysis predicted PVT1 negatively regulates miR-24 and KLF6 is a direct target of miR-24.

CONCLUSIONS

In a word, we observed PVT1 expression level was up-regulated in LPS- treated cardiac fibroblasts. PVT1 knockdown could alleviate LPS-induced biological behavior of cardiac fibroblasts through sponging miR-24 in vitro.