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- W4366192306 abstract "Ischemia-reperfusion (I/R) injury is an important in the pathogenesis of pressure ulcer. Reactive oxygen species (ROS) promotes ulcer formation through vascular injury and inflammatory cytokines production after I/R injury. We previously reported that induction of SOX2 in keratinocytes reprograms skin keratinocytes to an activated state and promotes wound healing via enhancement of EGFR signaling pathway. Further, recent studies revealed the interplay of ROS and EGFR signaling pathway in tumors. We aimed to evaluate the role of SOX2 in cutaneous I/R injury and the possible protective effect of SOX2 induction in keratinocytes on pressure ulcer formation in cutaneous I/R injury. Cutaneous I/R injury model was performed in keratinocyte specific SOX2 expressing mice (K14CreERTM/LSL-SOX2) and control mice. In SOX2 expressing mice, wound size at 5 days after reperfusion was suppressed to 56.3% of the control group (p=0.002). SOX2 in skin keratinocytes significantly suppressed the infiltrating inflammatory cells, apoptotic cells, vascular damage, and hypoxic areas in cutaneous I/R injury. mRNA levels of HO-1 and amphiregulin in I/R skin site were significantly upregulated in SOX2 mice. Antioxidant Nrf2 activity was significantly enhanced by SOX2 inductionin vivo and in vitro. Finally, recombinant amphiregulin treatment inhibited the pressure ulcer formation after cutaneous I/R injury to 48% of that in the control mice at 1 day after reperfusion (p=0.03). The oxidative stress-induced ROS production and apoptosis was inhibited by amphiregulin treatment in vitro. In conclusion, amphiregulin produced by SOX2 in keratinocytes showed protective effect on ulcer formation in cutaneous I/R injury. Amphiregulin administration might have therapeutic potential to be a new treatment for pressure ulcers." @default.
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- W4366192306 date "2023-05-01" @default.
- W4366192306 modified "2023-09-28" @default.
- W4366192306 title "1496 Transcription factor SOX2-induced amphiregulin inhibits pressure ulcer formation via suppressing oxidative stress after cutaneous ischemia-reperfusion in mice" @default.
- W4366192306 doi "https://doi.org/10.1016/j.jid.2023.03.1513" @default.
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