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
- extracorporeal membrane oxygenation
- oxidative stress
- signaling pathway
- single cell
- immune response
- cell proliferation
- pulmonary hypertension
- vascular endothelial growth factor
- long non coding rna
- inflammatory response
- mesenchymal stem cells
- intensive care unit
- dendritic cells
- end stage renal disease
- bone marrow
- endoplasmic reticulum stress
- diabetic rats
- drug induced
- stress induced
- current status