microRNA-103 promotes LPS-induced inflammatory injury by targeting c-Myc in HK-2 cells

Area of Science:

• Molecular Biology
• Cell Biology
• Renal Pathophysiology

Background:

• MicroRNAs (miRNAs) play crucial roles in disease pathogenesis.
• Lipopolysaccharide (LPS) is a potent inducer of inflammation and cellular damage in various cell types, including kidney cells.
• Understanding the specific roles of miRNAs in LPS-induced kidney injury is essential for developing targeted therapies.

Purpose of the Study:

• To investigate the influence of microRNA-103 (miR-103) on lipopolysaccharide (LPS)-induced inflammation and damage in HK-2 kidney cells.
• To elucidate the molecular mechanisms underlying miR-103's role in this cellular injury model.
• To explore the potential therapeutic implications of targeting miR-103.

Main Methods:

• HK-2 cells were treated with LPS to induce injury.
• Cell viability and apoptosis were assessed using CCK-8 assays and flow cytometry.
• Inflammation factors and protein expression were analyzed by ELISA, qRT-PCR, and Western blot.
• The interaction between miR-103 and c-Myc was confirmed using a luciferase reporter assay.

Main Results:

• LPS significantly reduced cell viability and proliferation-related proteins while increasing apoptosis and inflammatory cytokine production.
• LPS elevated miR-103 levels, which aggravated LPS-induced damage; conversely, a miR-103 inhibitor attenuated this damage.
• miR-103 negatively regulated c-Myc expression, and c-Myc silencing abolished the protective effects of the miR-103 inhibitor, indicating miR-103 mediates its effects through c-Myc.
• miR-103 influenced NF-κB and JAK/STAT pathways, also via c-Myc.

Conclusions:

• miR-103 mimics exacerbate LPS-induced inflammation and damage in HK-2 cells by silencing c-Myc.
• Inhibition of miR-103 demonstrates a protective effect against LPS-induced kidney cell injury.
• The miR-103/c-Myc axis represents a potential therapeutic target for managing LPS-induced kidney inflammation and damage.