Journal
REDOX BIOLOGY
Volume 41, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.redox.2021.101890
Keywords
HMGB1; Endothelium dependent relaxation; Angiogenesis; Ischemia; Reactive oxygen species; eNOS
Categories
Funding
- National Natural Science Foundation of China (NSFC) [81600248, 81800414]
- Natural Science Foundation of Hunan Province, China [2018JJ3744, 2018JJ3732]
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Recent studies have demonstrated that HMGB1 plays a crucial role in endothelial cells, influencing Akt/eNOS pathway and ROS production. Deletion of HMGB1 in endothelial cells resulted in decreased EDR and impaired angiogenesis, which could be partly rescued by superoxide dismutase.
Recent studies demonstrated HMGB1, an extracellular inflammation molecule, played an important role on endothelial cells. This study aimed to define the role and related mechanism of HMGB1 in endothelial cells. Endothelial-specific deletion of HMGB1(HMGB1ECKO) was generated and Akt/eNOS signaling, reactive oxygen species (ROS) production, endothelium dependent relaxation (EDR), and angiogenesis were determined in vitro and in vivo. Decreased activation of Akt/eNOS signaling, sprouting, and proliferation, and increased ROS production were evidenced in endothelial cells derived from HMGB1ECKO mice as compared with wild type controls. Decreased EDR and retarded blood flow recovery after hind limb ischemia were also demonstrated in HMGB1ECKO mice. Both impaired EDR and angiogenesis could be partly rescued by superoxide dismutase in HMGB1ECKO mice. In conclusion, intracellular HMGB1 might be a key regulator of endothelial Akt/eNOS pathway and ROS production, thus plays an important role in EDR regulation and angiogenesis.
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