Lnc-NEAT1 induces cell apoptosis and inflammation but inhibits proliferation in a cellular model of hepatic ischemia/reperfusion injury

Objective We aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury. Methods Human liver cells (HL-7702) were cultured under glucose-free and oxygen-free conditions to construct the I/R injury model. Expression of lnc-NEAT1 was detected in this model and in normal cells. Plasmids of control overexpression [NC(+)], lnc-NEAT1 overexpression [NEAT1(+)], control short hairpin (sh)RNA [NC(-)], and lnc-NEAT1 shRNA [NEAT1(-)] were transfected into HL-7702 cells and subsequently subjected to I/R treatment. Cell proliferation, apoptosis, apoptosis-related proteins, and inflammatory cytokines were assessed. Results Lnc-NEAT1 expression was elevated in the I/R group compared with the normal group. Cell proliferation was decreased in the NEAT1(+) group compared with the NC(+) group but increased in NEAT1(-) compared with NC(-). The apoptosis rate increased in the NEAT1(+) group compared with the NC(+) group but decreased in NEAT1(-) compared with NC(-). Western blot assay (detection of apoptosis-related proteins) showed similar results. Expression of interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha increased in the NEAT1(+) group compared with NC(+) but decreased in NEAT1(-) compared with NC(-). Conclusion Lnc-NEAT1 is overexpressed, induces cell apoptosis and inflammation, and inhibits proliferation during hepatic I/R injury.

Automated summary

The study revealed that overexpression of lnc-NEAT1 in hepatic ischemia/reperfusion injury model induced cell apoptosis and inflammation while inhibiting cell proliferation. Targeted interference of lnc-NEAT1 can reduce apoptosis rate and inflammatory cytokine expression, promoting liver cell proliferation.