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Area of Science:

  • Molecular Biology
  • Renal Physiology
  • Chronobiology

Background:

  • Melatonin exhibits protective effects in renal injury models.
  • The role of long noncoding RNAs (lncRNAs) in melatonin's renal signaling is largely unknown.
  • Understanding lncRNA regulation by melatonin is crucial for novel therapeutic strategies.

Purpose of the Study:

  • To identify and characterize melatonin-regulated lncRNAs in renal tubular epithelial cells (TECs).
  • To elucidate the mechanism by which melatonin influences TEC proliferation.
  • To investigate the therapeutic potential of the melatonin-NEAT1 axis in experimental kidney disease.

Main Methods:

  • Identification of nuclear enriched abundant transcript 1 (NEAT1) as a melatonin-upregulated lncRNA in TECs.
  • Mechanistic studies involving BMAL1/CLOCK heterodimers, gene promoter enrichment, and epigenetic modifications (H3K27ac, H3K4me1).
  • In vivo studies using experimental anti-glomerular basement membrane nephritis (anti-GBM MN) models to assess melatonin's effects on renal pathology and molecular markers.

Main Results:

  • Melatonin upregulates NEAT1 expression in TECs via the BMAL1/CLOCK pathway, enhancing BMAL1 stability and promoter enrichment.
  • NEAT1 promotes TEC proliferation by increasing histone acetylation and methylation at the MKI67 promoter.
  • Melatonin treatment ameliorated proteinuria, hypoalbuminemia, and fibrosis in MN kidneys, correlating with restored clock gene expression, NEAT1, and MKI67 levels.

Conclusions:

  • Melatonin regulates TEC proliferation through a novel BMAL1-NEAT1-MKI67 axis.
  • NEAT1 acts as a crucial mediator of melatonin's protective effects in renal injury.
  • This regulatory axis represents a potential therapeutic target for treating nephrotic syndrome and other kidney diseases.