microRNA-21 Aggravates Lipopolysaccharide-Induced Inflammation in MH7A Cells Through Targeting SNF5

Area of Science:

• Molecular Biology
• Cell Biology
• Immunology

Background:

• Inflammation plays a critical role in various diseases.
• MicroRNAs are key regulators of cellular processes, including inflammation.
• Lipopolysaccharide (LPS) is a potent inducer of inflammation.

Purpose of the Study:

• To investigate the role of microRNA-21 (miR-21) in LPS-induced inflammation in MH7A cells.
• To elucidate the underlying molecular mechanisms involving SNF5, NF-κB, and PTEN/PI3K/AKT pathways.

Main Methods:

• MH7A cells were treated with LPS and transfected with miR-21 mimic/inhibitor or SNF5.
• Cell viability was assessed using CCK-8 assay.
• Protein levels of inflammatory factors and signaling pathway components were measured by ELISA and Western blot.
• Gene expression was quantified by qRT-PCR.
• The interaction between miR-21 and SNF5 was confirmed via luciferase reporter assay.

Main Results:

• LPS treatment significantly increased cell viability, pro-inflammatory cytokines (IL-1β, IL-6), and activation of NF-κB and PTEN/PI3K/AKT pathways, while decreasing p-PTEN.
• LPS upregulated miR-21 expression; miR-21 mimic enhanced LPS effects, while miR-21 inhibitor alleviated them.
• miR-21 directly inhibited SNF5 expression, and SNF5 overexpression counteracted miR-21's pro-inflammatory effects.

Conclusions:

• MicroRNA-21 (miR-21) promotes LPS-induced inflammation in MH7A cells.
• miR-21 activates NF-κB and PTEN/PI3K/AKT signaling pathways by downregulating SNF5.
• Targeting miR-21 may offer a therapeutic strategy for inflammatory conditions.