Restoring and maintaining the function of endothelial cells is critical for acute respiratory distress syndrome (ARDS). Guanylate binding protein 1(GBP1) is proved to elevated in ARDS patients, but its role and mechanism remains unclear. The objective of this study is to investigate the internal mechanism of GBP1 in lung injury. Our study showed that when the LPS and IFN-γ induced human Pulmonary Microvascular Endothelial Cells (HPMECs) injury model was established, cell viability was significantly reduced, and the levels of GBP1 levels and inflammatory factors were significantly increased. When transfection with si-GBP1, low expression of GBP1 promoted cell proliferation and migration, and decreased the expression of downstream inflammatory factors. Furthermore, the inhibition of GBP1 significantly reduced the occurrence of cell pyroptosis and the expression of NLRP3 and STAT1. Our study indicated that GBP1 alleviates endothelial pyroptosis and inflammation through STAT1 / NLRP3/GSDMD signaling pathway, and GBP1 may be a new target in the treatment of lung injury in the future.
Keyphrases
- endothelial cells
- acute respiratory distress syndrome
- high glucose
- binding protein
- poor prognosis
- nlrp inflammasome
- oxidative stress
- signaling pathway
- extracorporeal membrane oxygenation
- cell proliferation
- mechanical ventilation
- single cell
- end stage renal disease
- pulmonary hypertension
- chronic kidney disease
- immune response
- risk assessment
- vascular endothelial growth factor
- inflammatory response
- mouse model
- newly diagnosed
- epithelial mesenchymal transition
- intensive care unit
- ejection fraction
- endoplasmic reticulum stress
- anti inflammatory
- dendritic cells
- induced pluripotent stem cells
- ionic liquid