YAP/TAZ Signaling Enhances Angiogenesis of Retinal Microvascular Endothelial Cells in a High-Glucose Environment

Curr Eye Res. 2024 May;49(5):524-532. doi: 10.1080/02713683.2024.2309217. Epub 2024 Feb 2.

Abstract

Purpose: Diabetic retinopathy (DR) is a major cause of irreversible blindness in the working-age population. Neovascularization is an important hallmark of advanced DR. There is evidence that Yes-associated protein (YAP)/transcriptional co-activator with a PDZ binding domain (TAZ) plays an important role in angiogenesis and that its activity is regulated by vascular endothelial growth factor (VEGF). Therefore, the aim of this study was to investigate the effect of YAP/TAZ-VEGF crosstalk on the angiogenic capacity of human retinal microvascular endothelial cells (hRECs) in a high-glucose environment.

Methods: The expression of YAP and TAZ of hRECs under normal conditions, hypertonic conditions and high glucose were observed. YAP overexpression (OE-YAP), YAP silencing (sh-YAP), VEGF overexpression (OE-VEGF) and VEGF silencing (sh-VEGF) plasmids were constructed. Cell counting kit-8 assay was performed to detect cells proliferation ability, transwell assay to detect cells migration ability, and tube formation assay to detect tube formation ability. The protein expression of YAP, TAZ, VEGF, matrix metalloproteinase (MMP)-8, MMP-13, vessel endothelium (VE)-cadherin and alpha smooth muscle actin (α-SMA) was measured by western blot.

Results: The proliferation of hRECs was significantly higher in the high glucose group compared with the normal group, as well as the protein expression of YAP and TAZ (p < 0.01). YAP and VEGF promoted the proliferation, migration and tube formation of hRECs in the high glucose environment (p < 0.01), and increased the expression of TAZ, VEGF, MMP-8, MMP-13 and α-SMA while reducing the expression of VE-cadherin (p < 0.01). Knockdown of YAP effectively reversed the above promoting effects of OE-VEGF (p < 0.01) and overexpression of YAP significantly reversed the inhibition effects of sh-VEGF on above cell function (p < 0.01).

Conclusion: In a high-glucose environment, YAP/TAZ can significantly promote the proliferation, migration and tube formation ability of hRECs, and the mechanism may be related to the regulation of VEGF expression.

Keywords: Diabetic retinopathy (DR); Yes-associated protein (YAP); human retinal microvascular endothelial cells (hRECs); transcriptional co-activator with a PDZ binding domain (TAZ); vascular endothelial growth factor (VEGF).

MeSH terms

  • Angiogenesis* / metabolism
  • Cell Proliferation
  • Diabetic Retinopathy* / genetics
  • Diabetic Retinopathy* / metabolism
  • Endothelial Cells / metabolism
  • Glucose / metabolism
  • Glucose / pharmacology
  • Humans
  • Matrix Metalloproteinase 13 / metabolism
  • Matrix Metalloproteinase 13 / pharmacology
  • Retina / metabolism
  • Retina / pathology
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • Transcriptional Coactivator with PDZ-Binding Motif Proteins* / metabolism
  • Vascular Endothelial Growth Factor A* / metabolism
  • YAP-Signaling Proteins* / metabolism

Substances

  • Glucose
  • Matrix Metalloproteinase 13
  • Transcription Factors
  • Vascular Endothelial Growth Factor A
  • YAP-Signaling Proteins
  • WWTR1 protein, human
  • Transcriptional Coactivator with PDZ-Binding Motif Proteins