Silence of lncRNA CHRF protects H9c2 cells against lipopolysaccharide-induced injury via up-regulating microRNA-221.

BACKGROUND:Cardiac hypertrophy related factor (CHRF), a newly recognized long non-coding RNA (lncRNA), is a central regulator in cardiac hypertrophy responses. This study attempted to show the potential role of lncRNA CHRF in bacterial infection caused myocarditis. METHODS:H9c2 cells were transfected with small interfering RNAs (siRNAs) specific for lncRNA CHRF alone or in combination with miR-221 inhibitor, and then subjected to lipopolysaccharide (LPS). The following parameters were measured: cell viability, apoptosis, reactive oxygen species generation, pro-inflammatory cytokines release, microRNA (miR)-221 expression and the activation of nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) pathways. RESULTS:Silence of lncRNA CHRF impeded the LPS injury to H9c2 cells, as cell viability was increased (p < .05), apoptosis was inhibited (p < .05), generation was decreased (p < .01), and the expression of interleukin (IL)-6 and tumor necrosis factor (TNF)-α was suppressed (p < .05). However, silence of lncRNA CHRF had no impacts on normal H9c2 cells growth (p > .05). miR-221 was negatively regulated by lncRNA CHRF (p < .01). LncRNA CHRF silence did not protect H9c2 cells against LPS when miR-221 was suppressed (p < .05 or p < .01). Also, the inhibitory effects of lncRNA CHRF silence on the activation of NF-κB and JNK pathways were flattened by miR-221 suppression (p < .05 or p < .01). CONCLUSION:These in vitro data collectively demonstrated that lncRNA CHRF silence protected H9c2 cells against LPS-induced injury via up-regulating miR-221 and modulating NF-κB and JNK pathways.

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