Engulfment of platelets delays endothelial cell aging via girdin and its phosphorylation.

Abstract

Endothelial cells are critical in angiogenesis and maintain the homeostasis of the blood‑brain barrier (BBB). Platelets (PLTs) are essential in vascular biology, including angiogenesis. The present study aimed to investigate the effect of PLTs on the aging of endothelial cells. Human brain microvascular endothelial cells (HBMECs) and human astrocytes were co‑cultured to mimic the BBB. Transmission electron microscopy was used to observe the engulfment of PLTs. Confocal microscopy was used to observe the co‑localization of PLTs, girders of actin filament (girdin) and phosphorylated (p‑)girdin. Senescence‑associated β‑galactosidase (β‑gal) staining, 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide and flow cytometry were performed to examine the cell senescence, viability and apoptosis, respectively. Transwell assays were performed to examine cell invasion and migration. Western blot analysis was performed to detect the expression of girdin, AKT and p‑AKT. PLTs delayed senescence, and promoted the viability and resistance to apoptosis of the HBMECs. Cell invasion and migration were enhanced by PLTs. In addition, girdin and p‑girdin were essential to the engulfment of HBMECs to PLTs. Mechanically, the inhibition of AKT signals reversed the effect of PLTs on HBMECs by increasing the activity of β‑gal, decreasing the cell viability, and inhibiting the invasion and migration of the HBMECs. The engulfment of PLTs assisted in delaying the aging of endothelial cells via girdin and p‑girdin, in which the AKT signal was involved. The present study indicated a potential strategy for delaying endothelial cell aging in the treatment of central nervous system diseases.