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Fig. 3 | Fluids and Barriers of the CNS

Fig. 3

From: Blue light exposure collapses the inner blood-retinal barrier by accelerating endothelial CLDN5 degradation through the disturbance of GNAZ and the activation of ADAM17

Fig. 3

Blue-light-mediated CLDN5 degradation is rely on ADAM17 activity. A Blue-light-mediated CLDN5 degradation could be prevented by 2 h pre-incubation of TAPI-2 (ADAM17 inhibitor, 10 μM). (*p < 0.05, ***p < 0.001, indicates statistical difference from the control treatment; # < 0.05, ##p < 0.01 indicates statistical difference from the blue-light-treated group). B bEnd.3 ADAM17-KD (stable clone) and HREC ADAM17-KD (transient transfection) were built. The knockdown of ADAM17 was accompanied by the CLDN5 protein accumulation, suggesting the involvement of ADAM17 activity in regular CLDN5 turnover. C Blue-light-mediated CLDN5 degradation was completely prevented in either bEnd.3 ADAM17-KD, or in HREC ADAM17-KD, as compared to that in wild-type. (*p < 0.05, **p < 0.01, ***p < 0.001, indicates statistical difference from the wild-type control treatment; ###p < 0.001 represents the significant difference from the blue-light-treated group). D In bEnd.3 ADAM17-KD clones, the enzymatic kinetics of ADAM17 was not induced in respond to blue light exposure. These data provide substantial evidence demonstrating the blue-light-mediated endothelial CLDN5 degradation, involving ADAM17 activation

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