Oxygen-glucose deprivation induces actin spillover in brain endothelial cells

Stroke is the leading cause of death and disability worldwide, and the mechanisms of stroke onset have not been fully elucidated. The research investigated how actin remodeling functions within brain microvascular endothelial cells (bEnd.3 cell²) when exposed to glucose-oxygen deprivation (OGD³) circumstances. OGD exposure for 6 h in bEnd.3 cell led to increased F-actin polymerization and actin overflow into the supernatant which demonstrated a disruption of intracellular actin balance. This process is mainly mediated by the cofilin and myosin light chain (MLC⁴) phosphorylation. Jasplakinolide further enhanced F-actin polymerization, while Latrunculin B inhibited actin polymerization and alleviated cellular damage. In conclusion, our research has revealed the crucial role of actin overflow driven by cofilin and MLC signals in brain endothelial cell injury, providing new insights into the pathophysiology of stroke.