Platelet Lysate Inhibits NF-κB Activation and Induces Proliferation and an Alert State in Quiescent Human Umbilical Vein Endothelial Cells Retaining Their Differentiation Capability

Injured blood vessel repair and blood circulation re-establishment are crucial events for
tissue repair. We investigated in primary cultures of human umbilical vein endothelial cells (HUVEC),
the eects of platelet lysate (PL), a cocktail of factors released by activated platelets following blood
vessel disruption and involved in the wound-healing process triggering. PL exerted a protective eect
on HUVEC in an inflammatory milieu by inhibiting IL-1-activated NF-B pathway and by inducing
the secretion of PGE2, a pro-resolving molecule in the wound microenvironment. Moreover, PL
enhanced HUVEC proliferation, without aecting their capability of forming tube-like structures on
matrigel, and activated resting quiescent cells to re-enter cell cycle. In agreement with these findings,
proliferation-related pathways Akt and ERK1/2 were activated. The expression of the cell-cycle
activator Cyclin D1 was also enhanced, as well as the expression of the High Mobility Group Box-1
(HMGB1), a protein of the alarmin group involved in tissue homeostasis, repair, and remodeling.
These in vitro data suggest a possible in vivo contribution of PL to new vessel formation after a
wound by activation of cells resident in vessel walls. Our biochemical study provides a rationale for
the clinical use of PL in the treatment of wound healing-related pathologies.