# PTIP inhibits proliferation, migration, and angiogenesis of retinal microvascular endothelial cells in a high-glucose environment

## TL;DR

This study shows that PTIP reduces harmful cell growth and inflammation in retinal cells exposed to high glucose, which is relevant to diabetic retinopathy.

## Contribution

The study reveals PTIP as a novel regulator of retinal cell behavior under high-glucose conditions, offering potential therapeutic insights for diabetic retinopathy.

## Key findings

- PTIP overexpression suppressed RMEC proliferation, migration, and tube formation in high-glucose environments.
- PTIP reduced inflammatory markers like IL-6, TNF-α, and oxidative stress in high-glucose-treated RMECs.
- PTIP knockdown increased VEGF, MDA, and other pro-angiogenic and inflammatory factors in RMECs.

## Abstract

The abnormal proliferation, migration, and angiogenesis of retinal microvascular endothelial cells (RMECs) are key pathological mechanisms involved in diabetic retinopathy (DR). This study aims to investigate the regulatory role of PAX interacting protein 1 (PTIP) in modulating proliferation, angiogenesis, and inflammatory responses in RMECs under high-glucose conditions. The levels of PTIP, VEGF, MDA, and SOD were measured in RMECs cultured under both normal and high-glucose conditions. A PTIP overexpression vector and a PTIP interference vector were constructed and transfected into RMECs exposed to high glucose. Cell proliferation was assessed using the CCK-8 assay, cell migration capacity was evaluated through wound healing assays, and tube formation ability was analyzed using Matrigel-based assays. Intracellular MDA and SOD levels were determined biochemically, while TNF-α and IL-6 concentrations in the culture supernatants were quantified by ELISA. The expression levels of EGR3, VEGF, MMP3, and MMP9 were detected using Western blotting and immunofluorescence techniques. The results showed that the expressions of PTIP and SOD were down-regulated in RMECs exposed to high glucose, whereas the levels of VEGF and MDA were up-regulated. Overexpression of PTIP in high-glucose-treated RMECs significantly suppressed cell proliferation, tube formation, and migration abilities. Additionally, it markedly reduced the levels of MDA, IL-6, TNF-α, EGR3, VEGF, MMP3, and MMP9 while increasing the level of SOD. Conversely, PTIP knockdown in RMECs under high-glucose conditions elicited opposite effects. Thus, overexpression of PTIP mitigated the impairment of proliferation, migration, and tube formation abilities, as well as reduced the inflammatory response induced by high glucose in RMECs.