p38 promoted retinal micro-angiogenesis through up-regulated RUNX1 expression in diabetic retinopathy

Biosci Rep. 2020 May 29;40(5):BSR20193256. doi: 10.1042/BSR20193256.

Abstract

Diabetic retinopathy (DR) is the most common microvascular complication of diabetes and is characterized by visible microvascular alterations including retinal ischemia-reperfusion injury, inflammation, abnormal permeability, neovascularization and macular edema. Despite the available treatments, some patients present late in the course of the disease when treatment is more difficult. Hence, it is crucial that the new targets are found and utilized in the clinical therapy of DR. In the present study, we constructed a DR animal model and a model in HRMECs to investigate the relationship between p38 and RUNX1 in retinal micro-angiogenesis in diabetic retinopathy. We found that p38 could promote retinal micro-angiogenesis by up-regulating RUNX1 expression in diabetic retinopathy. This suggested that the p38/ RUNX1 pathway could become a new retinal micro-angiogenesis target in DR treatment.

Keywords: Diabetic retinopathy; RUNX1; angiogenesis; p38.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Cell Line
  • Cell Proliferation
  • Core Binding Factor Alpha 2 Subunit / genetics
  • Core Binding Factor Alpha 2 Subunit / metabolism*
  • Diabetes Mellitus, Experimental / blood
  • Diabetes Mellitus, Experimental / complications
  • Diabetic Retinopathy / enzymology*
  • Diabetic Retinopathy / etiology
  • Diabetic Retinopathy / genetics
  • Diabetic Retinopathy / pathology
  • Endothelial Cells / drug effects
  • Endothelial Cells / enzymology*
  • Endothelial Cells / pathology
  • Glucose / toxicity
  • Humans
  • Male
  • Mice, Inbred C57BL
  • Retinal Neovascularization / enzymology*
  • Retinal Neovascularization / etiology
  • Retinal Neovascularization / genetics
  • Retinal Neovascularization / pathology
  • Retinal Vessels / drug effects
  • Retinal Vessels / enzymology*
  • Retinal Vessels / pathology
  • Signal Transduction
  • Up-Regulation
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Blood Glucose
  • Core Binding Factor Alpha 2 Subunit
  • RUNX1 protein, human
  • Runx1 protein, mouse
  • p38 Mitogen-Activated Protein Kinases
  • Glucose