Annexin A2 promotes development of retinal neovascularization through PI3K/ AKT signaling pathway

Curr Eye Res. 2022 Apr;47(4):579-589. doi: 10.1080/02713683.2021.2018467. Epub 2021 Dec 26.

Abstract

Purpose: Retinal Neovascularization (RNV) is a pathological characteristic of ocular diseases. Annexin A2 (ANXA2) plays important roles in RNV while the mechanism remains unclear. The study aimed to explore relationship between ANXA2 and PI3K/AKT signaling pathway in RNV.

Methods: We used human retinal vascular endothelial cells (HRECs) and oxygen-induced retinopathy (OIR) mice model to show ANXA2 can promote the development of RNV through PI3K/AKT signaling pathway. We divided HRECs into six groups by infecting lentivirus containing appropriate plasmid and adding corresponding solution. Assays showing ability of HRECs were performed in vitro. Mice were randomly divided into three groups and treated accordingly.

Results: Expression of ANXA2 and activity of PI3K/AKT signaling pathway in HRECs were detected. RNV and expression of ANXA2 in mice retinas were detected. Results showed that ANXA2 expression is positively related with RNV-forming ability of HRECs in vitro and development of RNV in vivo while low activity of PI3K/AKT signaling pathway could attenuate the role of ANXA2.

Conclusions: We can make ANXA2 and PI3K/ AKT signaling pathway as a promising target for the regulation of pathological neovascularization of the retina, which also provides a novel idea for effective prevention and treatment of diseases related to RNV in future.

Keywords: AKT; Annexin A2; PI3K; human retinal vascular endothelial cell; retinal neovascularization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Annexin A2* / metabolism
  • Annexin A2* / pharmacology
  • Disease Models, Animal
  • Endothelial Cells / metabolism
  • Mice
  • Oxygen / metabolism
  • Oxygen / toxicity
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Retinal Neovascularization* / metabolism
  • Signal Transduction

Substances

  • Annexin A2
  • Proto-Oncogene Proteins c-akt
  • Oxygen