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Hypoxic pulmonary hypertension (HPH) lacks effective pharmacologic treatments. Microarray-based gene expression indicates the crucial role of Cullin 5 (Cul 5) in HPH. This study showed that Cul 5 was upregulated in HPH patients and a murine model of HPH. In vitro, Cul 5 promoted the angiogenesis and adhesion capacity of human pulmonary artery endothelial cells (PAECs), which could be mitigated by Cul 5 inactivation mediated by pevonedistat or NEDD8 silence. In vivo, silencing of Cul 5 in the endothelium and Cul 5 inactivation by pevonedistat could also alleviate hypoxic vascular remodeling. Mechanistic research showed that Cul 5 participated in HPH pathogenesis via the TRAF6/NF-κB/HIF-1α/VEGF pathway. Inhibition of the TRAF6/NF-κB/HIF-1α/VEGF pathway could reverse Cul 5-induced human PAEC dysfunction. These findings demonstrate that Cul 5 is an important mediator of HPH via the TRAF6/NF-κB/HIF-1α/VEGF pathway firstly, and could be considered as a potential therapeutic target in the clinical treatment of HPH.
Pubmed ID: 37965157
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Mus musculus with name C57BL/6J from IMSR.
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View all literature mentionsThis monoclonal targets TRAF6
View all literature mentionsThis polyclonal targets Goat IgG
View all literature mentionsThis unknown targets
View all literature mentionsThis monoclonal targets Beta Actin
View all literature mentionsThis polyclonal targets IgG (H+L)
View all literature mentionsThis polyclonal targets Cullin 5/CUL-5
View all literature mentionsThis unknown targets Phospho-NF-kB p65 (Ser536)
View all literature mentionsThis polyclonal secondary targets IgG (H+L)
View all literature mentionsThis monoclonal targets CUL-5 (F-6)
View all literature mentionsThis monoclonal targets HIF1 alpha Mouse mAb
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