LncRNA SNHG16 reverses the effects of miR-15a/16 on LPS-induced inflammatory pathway

Area of Science:

• Molecular Biology
• Immunology
• Neonatal Research

Background:

• Neonatal sepsis presents a significant global health challenge with high incidence and mortality.
• MicroRNAs miR-15a and miR-16 are known modulators in neonatal sepsis, but their upstream regulatory mechanisms remain unclear.

Purpose of the Study:

• To investigate the role of long non-coding RNAs (lncRNAs) interacting with the miR-15a/16 cluster in neonatal sepsis.
• To elucidate the upstream molecular mechanism involving lncRNAs in neonatal sepsis.

Main Methods:

• Microarray analysis to identify downregulated lncRNAs in neonatal sepsis serum.
• Subcellular fractionation to determine SNHG16 localization.
• Mechanism investigations and rescue assays to assess SNHG16's ceRNA activity and its effect on the inflammatory pathway.

Main Results:

• SNHG16 was significantly downregulated in neonatal sepsis serum and primarily located in the cytoplasm, suggesting a ceRNA role.
• SNHG16 functions as a competing endogenous RNA (ceRNA) to upregulate TLR4, a target of miR-15a/16.
• SNHG16 reversed the effects of miR-15a/16 on the LPS-induced inflammatory pathway.

Conclusions:

• SNHG16 acts as a ceRNA, modulating the miR-15a/16 cluster in neonatal sepsis.
• This modulation affects the LPS-induced inflammatory pathway, offering potential therapeutic targets.