Key result
Overexpression of LINC01093 suppressed hepatocyte apoptosis and promoted proliferation in an alcoholic hepatitis mouse model by inhibiting the ICAM-1-mediated NF-κB signaling pathway.
Why the study?
To clarify the specific role and underlying mechanism of differentially expressed LINC01093 and ICAM-1 in alcoholic hepatitis.
LINC01093 overexpression protects against alcoholic hepatitis by inhibiting the ICAM-1-mediated NF-κB signaling pathway in a preclinical model.
Hypothesis-generating for LINC01093 modulation in alcoholic hepatitis; requires human validation before any clinical consideration.
The long noncoding RNAs (lncRNAs) have been proven to be involved in the development of alcoholic hepatitis (AH), which has been regarded as a severe form of acute liver injury with a high mortality rate. Through the GEO database, the differentially expressed LINC01093 and intercellular cell adhesion molecule-1 (ICAM-1) were identified in AH. Then, to clarify their specific role and underlying mechanism in AH, we constructed an AH mouse model by using Lieber-Decarli alcoholic feed. It was found that LINC01093 was poorly expressed and ICAM-1 was highly expressed in AH mice. After that, the interactions among LINC01093, ICAM-1, and NF-κB signaling pathway were explored, which verified that LINC01093 could target ICAM-1 and inhibit the NF-κB signaling pathway. Finally, after the hepatocytes were isolated from AH mice, the expression of LINC01093 was up- or downregulated or that of ICAM-1 was silenced to evaluate their effect on cell viability and apoptosis. The corresponding results demonstrated that after overexpression of LINC01093 or silencing of ICAM-1, cell viability was increased and cell apoptosis was reduced in the hepatocytes of AH mice. Moreover, the silencing of LINC01093 was observed to inhibit the viability and promote the apoptosis of hepatocytes of AH mice. Altogether, these results provide evidence that overexpression of LINC01093 could effectively suppress hepatocyte apoptosis and promote proliferation by inhibiting the ICAM-1-mediated NF-κB signaling pathway, thus playing a functional role in AH and hepatic fibrosis.
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Shi et al. (2019) studied Alcoholic hepatitis. LINC01093 overexpression vs. Control / LINC01093 downregulation was evaluated on Hepatocyte viability and apoptosis. Overexpression of LINC01093 suppressed hepatocyte apoptosis and promoted proliferation in an alcoholic hepatitis mouse model by inhibiting the ICAM-1-mediated NF-κB signaling pathway.
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