PRDX1 Suppresses Oxidative Stress and Senescence in HUVECs by Stabilizing TRAF4.

SummaryThis study aimed to verify the effect of peroxiredoxin 1 (PRDX1) in wound healing. PRDX1 and tumor necrosis factor receptor-associated factor 4 (TRAF4) expressions in human umbilical vein endothelial cells (HUVECs) were assessed by real-time quantitative PCR and Western blot. Cell proliferation, migration, and angiogenesis were assessed by cell counting kit-8, wound healing, and tube formation assay. The reactive oxygen species level was measured using 2'-7'-dichlorodihydrofluorescein diacetate. Senescence-associated β-galactosidase staining assay was used to detect cells senescence. The relationship among PRDX1, TRAF4, and UBE3A was determined by co-immunoprecipitation. Upregulation of PRDX1 promoted the proliferation, migration, and angiogenesis of HUVECs. Meanwhile, PRDX1 overexpression inhibited oxidative stress and senescence of HUVECs by H(2)O(2)-induced. Furthermore, overexpression of PRDX1 inhibited the degradation of TRAF4 to activate PI3K/AKT/VEGF axis via binding to UBE3A. The effect of PRDX1 on H(2)O(2)-induced oxidative stress and senescence was reversed by TRAF4 silence. The promotion of PRDX1 on proliferation, migration, and angiogenesis was canceled by knockdown of TRAF4. PRDX1 inhibited oxidative stress and senescence via restraining the degradation of TRAF4 by binding to UBE3A, eventually accelerating wound healing.