GDF15 helps cause radiation-related aging in human blood vessel cells through a stress-related p16 pathway

GDF15 levels were increased during cellular senescence induced by ionizing radiation in human aortic endothelial cells.

• Downregulation of GDF15 in human aortic endothelial cells partially prevented cellular senescence triggered by ionizing radiation.
• Recovery of cell proliferation and reduced senescence-associated β-galactosidase staining were observed with GDF15 downregulation.
• Upregulation of GDF15 induced cellular senescence, evidenced by G0/G1 cell cycle arrest and increased senescence-associated β-galactosidase staining.
• GDF15-induced cellular senescence occurred in cells with p16 knockdown but not in those with p53 knockdown.
• GDF15 expression in endothelial cells generated reactive oxygen species, activating signaling pathways associated with cellular senescence.

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