Blood-brain barrier (BBB) dysfunction is presented during traumatic brain injury (TBI) and is dependent upon the activation of the NLRP3/Caspase-1 inflammasome pathway. MicroRNA (miRNA) was proved to inhibit signaling pathway activation by targeting gene expression and we predicated in the database that miR-29a targets to NLRP3. Herein, this study aims to define the regulating role of miR-29a in NLRP3 expression and NLRP3/Caspase-1 inflammasome activation in TBI-induced BBB dysfunction. Our results indicated that miR-29a-5p alleviates TBI-induced the increased permeability of endothelial cell and BBB via suppressing NLRP3 expression and NLRP3/Caspase-1 inflammasome activation, providing a promising strategy for relieving TBI via inhibiting NLRP3/Caspase-1 inflammasome activation.
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Figure S1: miR-29a-3p or miR-29a-5p mimics significantly improved the expression of miR-29a-3p or miR-29a-5p respectively in mouse bEnd.3 cells. *** p < 0.001 compared with miNC.
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Posted 23 Mar, 2021
On 17 Mar, 2021
On 15 Mar, 2021
On 14 Mar, 2021
On 14 Mar, 2021
On 14 Mar, 2021
Posted 23 Mar, 2021
On 17 Mar, 2021
On 15 Mar, 2021
On 14 Mar, 2021
On 14 Mar, 2021
On 14 Mar, 2021
Blood-brain barrier (BBB) dysfunction is presented during traumatic brain injury (TBI) and is dependent upon the activation of the NLRP3/Caspase-1 inflammasome pathway. MicroRNA (miRNA) was proved to inhibit signaling pathway activation by targeting gene expression and we predicated in the database that miR-29a targets to NLRP3. Herein, this study aims to define the regulating role of miR-29a in NLRP3 expression and NLRP3/Caspase-1 inflammasome activation in TBI-induced BBB dysfunction. Our results indicated that miR-29a-5p alleviates TBI-induced the increased permeability of endothelial cell and BBB via suppressing NLRP3 expression and NLRP3/Caspase-1 inflammasome activation, providing a promising strategy for relieving TBI via inhibiting NLRP3/Caspase-1 inflammasome activation.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
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