Activin A Prevents Hyperresponsiveness to Vascular Endothelial Growth Factor in Pathologic Blood Vessels by Perturbing the Trafficking of Activated Vascular Endothelial Growth Factor Receptor 2.

ABSTRACT: Although quality-of-life compromising afflictions, such as diabetic retinopathy (DR), are driven by vascular endothelial growth factor (VEGF), there is a growing appreciation that the concentration of VEGF is not the only influencer of vascular dysfunction within the retina. Herein, activin A (activin), a ligand of the transforming growth factor-β superfamily, attenuated VEGF-induced vascular endothelial-cadherin disorganization, pore formation, and permeability of primary human retinal endothelial cells. Efforts to further investigate the mechanism of this phenomenon revealed that activin reduced the expression of Rab11, which was required for the activin effect. The activin effect was not observed in cells with suppressed expression of the endosomally localized protein tyrosine phosphata

SUBMITTER: Baccouche B 

PROVIDER: S-EPMC12489374 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature