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Exosomes Derived From Mesenchymal Stem Cells Modulate miR-126 to Ameliorate Hyperglycemia-Induced Retinal

Wei Zhang1, Yang Wang2, Yichun Kong1

  • 1Tianjin Eye Hospital, Tianjin Key Lab of Ophthalmology and Visual Science, Tianjin Eye Institute, Clinical College of Ophthalmology, Tianjin Medical University, Tianjin, China.

Investigative Ophthalmology & Visual Science
|January 19, 2019
PubMed
Abstract

Insights

Mesenchymal stem cell-derived exosomes (MSC-Exos) carrying microRNA-126 (miR-126) effectively reduce retinal inflammation caused by high blood sugar. This is achieved by suppressing the HMGB1 signaling pathway, offering a potential therapeutic strategy for diabetic retinopathy.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Biochemistry

Background:

  • Diabetic retinopathy is a leading cause of blindness, characterized by retinal inflammation.
  • Hyperglycemia exacerbates retinal inflammation through pathways like HMGB1 and the NLRP3 inflammasome.
  • Mesenchymal stem cell-derived exosomes (MSC-Exos) show therapeutic potential, but their specific role in regulating diabetic retinal inflammation needs clarification.

Purpose of the Study:

  • To investigate if MSC-Exos can modulate hyperglycemia-induced retinal inflammation.
  • To determine the role of microRNA-126 (miR-126) transfer from MSC-Exos in this process.

Main Methods:

  • Human umbilical cord-derived MSC-Exos were isolated and engineered to overexpress miR-126.
  • These exosomes were administered to diabetic rats and co-cultured with high glucose-treated human retinal endothelial cells (HRECs).
  • Inflammatory markers, HMGB1, and NLRP3 inflammasome activity were assessed using RT-PCR, Western blotting, and immunohistochemistry.

Main Results:

  • Hyperglycemia significantly increased retinal inflammation and inflammatory markers (caspase-1, IL-1β, IL-18) in vivo and in vitro.
  • MSC-Exos administration reversed these inflammatory effects.
  • MSC-Exos overexpressing miR-126 demonstrated superior suppression of the HMGB1 signaling pathway and NLRP3 inflammasome activity compared to control MSC-Exos.

Conclusions:

  • miR-126 delivered via MSC-Exos effectively reduces hyperglycemia-induced retinal inflammation.
  • The mechanism involves the downregulation of the HMGB1 signaling pathway.
  • This highlights a potential therapeutic application of miR-126-enriched MSC-Exos for diabetic retinopathy.

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