Long Non-Coding RNA Expression Profile Alteration Induced by Titanium Dioxide Nanoparticles in HepG2 Cells

Area of Science:

• Hepatology
• Nanotoxicology
• Epigenetics

Background:

• The liver is a primary target for oral titanium dioxide nanoparticle (TiO2 NP) exposure.
• The precise mechanisms underlying TiO2 NP-induced liver toxicity remain incompletely understood.

Purpose of the Study:

• To investigate the impact of TiO2 NPs on long non-coding RNA (lncRNA) expression profiles in hepatocytes.
• To elucidate potential mechanisms of hepatotoxicity using bioinformatics analysis.

Main Methods:

• Human hepatocellular carcinoma cells (HepG2) were exposed to varying doses of TiO2 NPs (0-200 μg/mL) for 48 hours.
• RNA sequencing was performed to identify differentially expressed lncRNAs.
• lncRNA-mRNA networks and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were analyzed.

Main Results:

• A total of 46,759 lncRNAs were identified, with 129 found to be differentially expressed.
• KEGG pathway analysis revealed enrichment in Hedgehog signaling, Vasopressin-regulated water reabsorption, and Glutamatergic synapse pathways.
• Two specific lncRNA-mRNA interactions (NONHSAT256380.1-JRK and NONHSAT173563.1-SMIM22) were validated.

Conclusions:

• TiO2 NP exposure induces significant alterations in the lncRNA expression profile of hepatocytes.
• Epigenetic modifications, particularly involving lncRNAs, are implicated in the mechanism of TiO2 NP-induced hepatotoxicity.