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High glucose-induced circHIPK3 downregulation mediates endothelial cell injury

Ying Cao1, Guohai Yuan1, Ye Zhang1

  • 1Nutrition Department, Kunshan Traditional Chinese Medicine Hospital, Kunshan, China.

Biochemical and Biophysical Research Communications
|November 21, 2018
PubMed

Insights

High glucose damages vascular cells by downregulating circular RNA HIPK3 (circHIPK3). Restoring circHIPK3 levels protects against cell death, suggesting a therapeutic target for diabetic vascular injury.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • High glucose (HG) is a key factor in diabetic complications, leading to vascular endothelial cell injury.
  • The precise molecular mechanisms underlying HG-induced endothelial cell damage remain incompletely understood.
  • Circular RNAs (circRNAs) are emerging as critical regulators in various biological processes, including cellular responses to metabolic stress.

Purpose of the Study:

  • To investigate the role of circular RNA HIPK3 (circHIPK3) in high glucose-induced vascular endothelial cell injury.
  • To elucidate the molecular pathway involving circHIPK3 and its interaction with microRNA-124 (miR-124) in diabetic vascular complications.
  • To explore the therapeutic potential of targeting the circHIPK3-miR-124 axis for treating diabetic vascular disease.

Main Methods:

  • Quantitative real-time PCR to assess circHIPK3 and miR-124 expression levels in endothelial cells.
  • Lentiviral vectors and small interfering RNA (siRNA) for circHIPK3 overexpression and silencing, respectively.
  • Adeno-associated virus (AAV) vectors for miR-124 inhibition.
  • Cell viability assays and apoptosis detection (e.g., TUNEL assay, Annexin V staining) to evaluate endothelial cell injury.

Main Results:

  • circHIPK3 expression was significantly downregulated in human umbilical vein endothelial cells (HUVECs) and primary human aortic endothelial cells (HAECs) exposed to high glucose, as well as in cells from diabetic patients.
  • Overexpression of circHIPK3 protected endothelial cells against HG-induced cell death and apoptosis, while circHIPK3 silencing exacerbated these effects.
  • HG-induced downregulation of circHIPK3 led to the accumulation of miR-124, and inhibition of miR-124 using AAV vectors conferred protection against HG-induced endothelial cell injury.

Conclusions:

  • circHIPK3 downregulation is a critical mediator of high glucose-induced vascular endothelial cell injury.
  • The circHIPK3-miR-124 pathway plays a significant role in the pathogenesis of diabetic vascular complications.
  • Targeting the circHIPK3-miR-124 axis represents a promising novel therapeutic strategy for diabetic-associated vascular injury.

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