Brain research · 2026
IGFBP7 protects against endothelial apoptosis and blood-brain barrier disruption following oxygen-glucose deprivation/reoxygenation.
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Zhu Yuyi, Cui Ting, Chen Mingxi, Xu Mangmang, Sima Xiutian, Wang Deren
Аннотация
BACKGROUND: The blood-brain barrier (BBB) is a critical interface maintained by cerebral microvascular endothelial cells, which rely on tight junction (TJ) proteins like ZO-1 and occludin to regulate permeability. Following ischemic stroke, BBB disruption and subsequent cerebral edema are major contributors to poor clinical outcomes. Insulin-like growth factor-binding protein 7 (IGFBP7) is highly expressed in these endothelial cells and has been implicated in both BBB formation and vascular repair. However, its specific role in stroke-induced endothelial injury has remained inconclusive.
METHODS AND RESULTS: In this study, we investigated the function of IGFBP7 in an in vitro model of oxygen-glucose deprivation and reoxygenation (OGD/R) using mouse microvascular endothelial (bEnd.3) cells. We manipulated IGFBP7 levels through overexpression and siRNA-mediated silencing. Our results show that OGD/R treatment significantly decreased IGFBP7 expression, which led to increased BBB permeability, degradation of tight junction proteins, and cellular apoptosis. Importantly, overexpressing IGFBP7 mitigated these effects, restoring the expression of ZO-1 and reducing apoptosis. Conversely, silencing IGFBP7 exacerbated both tight junction protein degradation and cell apoptosis.
CONCLUSION: Endothelial IGFBP7 exerts a protective role in ischemic stroke by blunting OGD/R-mediated BBB damage and thus, it may represent an interesting novel therapeutic target to be explored in future clinical investigation.
METHODS AND RESULTS: In this study, we investigated the function of IGFBP7 in an in vitro model of oxygen-glucose deprivation and reoxygenation (OGD/R) using mouse microvascular endothelial (bEnd.3) cells. We manipulated IGFBP7 levels through overexpression and siRNA-mediated silencing. Our results show that OGD/R treatment significantly decreased IGFBP7 expression, which led to increased BBB permeability, degradation of tight junction proteins, and cellular apoptosis. Importantly, overexpressing IGFBP7 mitigated these effects, restoring the expression of ZO-1 and reducing apoptosis. Conversely, silencing IGFBP7 exacerbated both tight junction protein degradation and cell apoptosis.
CONCLUSION: Endothelial IGFBP7 exerts a protective role in ischemic stroke by blunting OGD/R-mediated BBB damage and thus, it may represent an interesting novel therapeutic target to be explored in future clinical investigation.