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MiR-137 promotes cell growth and inhibits extracellular matrix protein expression in H2O2-induced human trabecular

Liang Wang1, Ying Tian1, Yan Cao1

  • 1Department of Ophthalmology, Xi'an NO.1 Hospital, Xi'an, 710002, China.

Neuroscience Letters
|April 18, 2021
PubMed

Insights

MicroRNA-137 (miR-137) plays a crucial role in glaucoma by protecting trabecular meshwork cells. Restoring miR-137 levels may offer a new therapeutic strategy for glaucoma treatment.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • Glaucoma is a leading cause of irreversible blindness, characterized by progressive optic neuropathy.
  • MicroRNAs (miRNAs) are implicated in regulating trabecular meshwork (TM) cellular functions relevant to glaucoma pathogenesis.
  • The specific role of miR-137 in glaucoma and its underlying molecular mechanisms require further elucidation.

Purpose of the Study:

  • To investigate the role of miR-137 in the context of glaucoma.
  • To elucidate the molecular mechanisms by which miR-137 influences trabecular meshwork cell behavior.
  • To explore the potential of miR-137 as a therapeutic target for glaucoma.

Main Methods:

  • Utilized hydrogen peroxide (H₂O₂)-induced human trabecular meshwork cells (HTMCs) as a model system.
  • Assessed the expression levels of miR-137 under oxidative stress conditions.
  • Investigated the effects of miR-137 overexpression on cell viability, apoptosis, and extracellular matrix (ECM) protein expression.
  • Examined the interaction of miR-137 with the src gene and its impact on the YAP/TAZ signaling pathway.

Main Results:

  • miR-137 expression was found to be downregulated in H₂O₂-induced HTMCs.
  • Overexpression of miR-137 attenuated H₂O₂-induced cell growth inhibition and apoptosis.
  • miR-137 overexpression inhibited elevated extracellular matrix (ECM) protein expression and blocked YAP/TAZ activation by directly targeting src.
  • Modulation of src or YAP/TAZ pathway partially reversed the protective effects of miR-137.

Conclusions:

  • miR-137 promotes cell growth and inhibits ECM protein expression in H₂O₂-stressed HTMCs.
  • The protective effects of miR-137 are mediated through the YAP/TAZ pathway by targeting src.
  • miR-137 represents a potential novel therapeutic target for managing glaucoma.
Keywords:
Extracellular matrixGlaucomaOxidative stressmiR-137

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