LncRNA HOTAIR promotes LPS-induced inflammatory responses by activating the NF-κB pathway

Area of Science:

• Molecular Biology
• Immunology
• Respiratory Medicine

Background:

• Acute lung injury (ALI) involves excessive inflammation driven by the NF-κB signaling pathway.
• Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in inflammatory diseases.

Purpose of the Study:

• To investigate the role of the lncRNA HOTAIR in lipopolysaccharide (LPS)-induced ALI.
• To evaluate HOTAIR as a potential therapeutic target for ALI.

Main Methods:

• Utilized A549 cell and murine models of LPS-induced lung injury.
• Assessed HOTAIR expression, cell viability, pro-inflammatory cytokine levels (IL-1β, IL-6, TNF-α).
• Analyzed NF-κB signaling pathway activation (IκBα and p65 phosphorylation, p65 nuclear translocation) and HOTAIR knockdown effects.

Main Results:

• LPS increased HOTAIR expression, reduced cell viability, and elevated pro-inflammatory cytokines in A549 cells.
• HOTAIR overexpression amplified NF-κB signaling; HOTAIR silencing reversed these effects.
• In vivo, HOTAIR knockdown mitigated lung injury, reduced inflammation, and suppressed NF-κB activation in mice.

Conclusions:

• HOTAIR contributes to NF-κB-driven inflammatory injury in ALI.
• HOTAIR plays a regulatory role in ALI pathogenesis.
• Targeting HOTAIR presents a potential therapeutic avenue for ALI.