Extended Data Fig. 7: Additional characterization of StcE treatment in young mice.
From: Glycocalyx dysregulation impairs blood–brain barrier in ageing and disease
a) Overview of luminal mucin-domain glycoprotein degradation paradigm using 24-h StcE treatment. b) Whole brain images of sulfo-NHS-biotin leakage in StcE-treated mice at 24 h. Scale bar = 1 mm. c) Quantification of cortical vessel permeability to sulfo-NHS-biotin in (b) (n = 4 mice per group; two-sided t-test; mean ± s.e.m.). d) Mucin domain, heparan sulfate, chondroitin sulfate, and hyaluronan expression in acutely isolated microvessels from 24-h saline- and StcE-treated mice. Scale bar = 10 µm. e) Quantification of (d) (n = 3 mice per group, two-sided t-test; mean± s.e.m.). f) Sulfo-NHS-biotin leakage (white) from blood vessels in different brain regions of 48-h StcE-treated mice. Scale bar = 50 µm. g) Quantification of sulfo-NHS-biotin permeability in different brain regions in saline- and 48-h StcE-treated mice (n = 4 mice per group; two-sided t-test; mean ± s.e.m.). h) Additional brains from 48-h StcE-treated mice exhibiting hemorrhaging (n = 4 mice per group). i) H&E images of lung, liver, and kidney in saline and 48-h StcE-treated mice. Scale bar = 50 µm. j) Luminex quantification of major inflammatory cytokines in plasma from young mice following saline, StcEE447D, and StcE treatment. (n = 4 mice per group, one-way ANOVA with Dunnett’s post hoc test; mean ± s.e.m.).
