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Abstract Details
SARS-CoV-2 N protein interacts with SLC7A11 to cause ferroptosis in acute lung injury.
Liu, Yi (Y);Tang, Hui (H);Xu, Pan (P);Zhou, Xiaoqi (X);Li, Shiying (S);
BACKGROUND: The nucleocapsid protein (N protein) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is elevated in bodily fluids at the onset of infection and has recently been found to have a direct role in lung damage. However, the exact mode of action of the N protein in acute lung injury is still unknown.
METHOD: Recombinant N protein was used to treat mice and A549 cells in vivo and in vitro. Enzyme-linked immunosorbent assay and hematoxylin and eosin staining were used to detect the levels of inflammatory factors and lung damage in lung tissue. The total iron and Fe contents and the expression of ferroptosis markers in mouse lung tissues and cells were detected. Co-immunoprecipitation detects the binding of N protein and solute carrier family 7 member 11 (SLC7A11). Replenishment experiments were conducted by activating SLC7A11 to study the effect of SLC7A11 on N protein-induced lung injury.
RESULT: Recombinant N protein caused acute lung injury and lung inflammation, increased total iron and Fe contents in vivo and in vitro, promoted the expression of ACSL4, inhibited the expression of GPX4 and FTH1, and triggered ferroptosis. Recombinant N protein can interact with SLC7A11, and activating SLC7A11 can reverse N protein-induced ferroptosis and acute lung injury.
CONCLUSION: SARS-CoV-2 N protein can directly interact with SLC7A11 to cause ferroptosis, which produces a lot of inflammatory factors and results in lung injury in mice.
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