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MiR-29 regulates retinopathy in diabetic mice via the AMPK signaling pathway

B-W Zhao1, H-Y Dai, L-N Hao

  • 1Department of Ophthalmology, Hongqi Hospital Affiliated to Mudanjiang Medical University, Mudanjiang, China. 252831514@qq.com.

European Review for Medical and Pharmacological Sciences
|May 23, 2019
PubMed
Abstract

Insights

Diabetic retinopathy in mice is linked to decreased micro-ribonucleic acid (miR)-29 and altered adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling. Restoring miR-29 may offer a therapeutic target for diabetic eye disease.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Diabetology

Background:

  • Diabetic retinopathy (DR) is a leading cause of vision loss.
  • Micro-ribonucleic acids (miRNAs) play crucial roles in cellular processes and disease pathogenesis.
  • The adenosine 5'-monophosphate-activated protein kinase (AMPK) pathway is implicated in metabolic regulation and cellular stress responses.

Purpose of the Study:

  • To investigate the role of micro-ribonucleic acid (miR)-29 in diabetic retinopathy (DR).
  • To examine the influence of miR-29 on the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway in diabetic mice.
  • To assess the impact of miR-29 on retinal function and apoptosis in a diabetic mouse model.

Main Methods:

  • Established a diabetic mouse model and compared it to a normal control group.
  • Evaluated retinal function using electroretinography (ERG) to measure b-wave latency and amplitude.
  • Assessed expression of apoptosis-related proteins (Bcl-2, Bax), p-AMPK, p-mTOR, and miR-29 using immunohistochemistry, Western blotting, and quantitative Polymerase Chain Reaction (qPCR).
  • Quantified cell apoptosis via terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay.

Main Results:

  • Diabetic mice exhibited prolonged b-wave latency and decreased amplitude compared to controls (p<0.05).
  • Increased Bax and decreased Bcl-2 expression, alongside reduced p-AMPK and elevated p-mTOR levels, were observed in diabetic mice (p<0.05).
  • A significant decrease in miR-29 expression and a marked increase in retinal cell apoptosis were found in the diabetic model group (p<0.05).

Conclusions:

  • Downregulation of miR-29 is associated with diabetic retinopathy in mice.
  • The AMPK signaling pathway is dysregulated in diabetic retinopathy, with decreased p-AMPK and increased p-mTOR.
  • miR-29 may play a protective role in diabetic retinopathy, and its modulation could be a potential therapeutic strategy.

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