Functionally, as observed in Atg5 ΔEC mice, IR-stimulated postcapillary venular ECs of Atg16L1 E230 mice exhibited significant enrichment (>40%) of PECAM-1 at cell-cell contacts as compared to WT littermates ( Figures 6 E–6G) and showed a trend toward increased (>20%) VE-cadherin accumulation at junctions ( Figures 6 E, S6 A, and S6B).
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Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation.
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