MicroRNA-155 expression is associated with pulpitis progression by targeting SHIP1.

Area of Science:

• Oral Biology
• Molecular Biology
• Immunology

Background:

• Pulpitis is a common oral inflammatory condition with poorly understood pathogenic mechanisms.
• MicroRNA-155 (miR-155) expression is associated with dental pulpal inflammation in vivo and in vitro.

Purpose of the Study:

• To elucidate the role of miR-155 in regulating dental pulpal inflammation.
• To identify the molecular targets and signaling pathways involved in miR-155-mediated inflammation.

Main Methods:

• Utilized LPS-stimulated odontoblast cell lines (MDPC-23) and miR-155 knockout mice.
• Performed bioinformatics analysis to identify miR-155 targets.
• Investigated the effects of miR-155 modulation on pro-inflammatory cytokines (IL-1β, IL-6), SHIP1 expression, and PI3K/AKT signaling pathway activation.

Main Results:

• miR-155 acts as a positive regulator of inflammation, increasing IL-1β and IL-6 production.
• SHIP1 was identified as a direct target of miR-155 in odontoblasts.
• miR-155 inhibition downregulated inflammation, while targeting SHIP1 reversed this effect.
• The PI3K/AKT pathway was activated by miR-155 mimics and si-SHIP1, and inhibited by miR-155 inhibitors.

Conclusions:

• miR-155 plays a critical role in regulating dental pulpal inflammation.
• This regulation occurs via targeting SHIP1 and modulating the PI3K/AKT signaling pathway.
• These findings reveal a novel mechanism for pulpitis pathogenesis and suggest potential therapeutic targets.