Glutamine Depletion Induced Senescence-Associated β-Galactosidase Activity and Impaired Functional Properties of Ea.hy926 Endothelial Cells

Glutamine is a conditionally essential amino acid that is important for endothelial homeostasis, while endothelial cell dysfunction is associated with altered glutamine metabolism and shifts toward stress-responsive pathways. We investigated the role of glutamine and senescence-associated beta-galactosidase (SA-β-gal) activity in Ea.hy926 endothelial cells (ECs), together with supportive functional activity assays. We found that glutamine depletion induced a progressive decline in endothelial function. Specifically, glutamine-depleted ECs exhibited increased SA-β-gal activity, accompanied by impaired proliferative capacity, disrupted cellular morphogenesis, increased promyelocytic cell adhesion, and diminished ability to promote host tissue proliferation and EC morphogenesis in a zebrafish xenograft model. These findings suggest that glutamine availability is crucial for maintaining endothelial integrity and functional competence.