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Fig. 7 | Molecular Brain

Fig. 7

From: Meningitic Escherichia coli α-hemolysin aggravates blood–brain barrier disruption via targeting TGFβ1-triggered hedgehog signaling

Fig. 7

The HlyA-triggered Ca2+ influx and PKA activation accounted for the infection-caused ZO-1 and Gli2 reduction. A, B Ca2+ influx of hBMECs upon infection of RS218-WT, RS218-ΔhlyA, and RS218-ΔhlyA-phlyA strains for 2 h determined by the Fluo-3-AM probed through the fluorescence microscopy (A) and flow cytometry (B). The assay was performed with 3 replicates, and data were presented as mean ± SEM. ** p < 0.01. ns, no significance. Scale bar indicated 100 μm. Cells in Blank group were not treated. Cells in Control group, RS218-WT group, RS218-ΔhlyA group, and RS218-ΔhlyA-phlyA group were loaded with Fluo-3-AM and treated as indicated. C The expression of ZO-1 and Gli2 in hBMECs upon RS218 infection, as well as upon infection with pre-treatment of Ca2+ chelator EGTA (5 mM) or PKA activity inhibitor H89 (20 µM). D PKA activity in hBMECs upon the infection of RS218-WT, RS218-ΔhlyA, and RS218-ΔhlyA-phlyA strains, and upon the infection in the presence of EGTA (5 mM)

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