Fig. 6 | Scientific Reports

Fig. 6

From: SLC37A4, gene responsible for glycogen storage disease type 1b, regulates gingival epithelial barrier function via JAM1 expression

Fig. 6

SLC37A4 knockout dampens epithelial barrier function of gingival epithelial tissues. (a) Schematic image of culture-insert system. WT or ΔSLC37A4 gingival epithelial tissues with or without overexpression of JAM1 were cultured in the upper compartments. FITC-labeled tracers were then added to culture medium in each upper compartment. Following 3 h of incubation, transmission of a tracer from the upper to lower compartment was analyzed by spectrometry. (b) Confocal microscopic cross-sectional images of 3D-tissue model of IHGE cells. WT and ΔSLC37A4 gingival epithelial tissues with or without overexpression of JAM1 on coverslips were fixed, stained with DAPI (cyan) and Alexa Fluor 633-conjugated phalloidin (gray), and analyzed using confocal microscopy. Scale bars, 30 μm. (c, d) Permeability of gingival epithelial tissues to FITC-P. gingivalis LPS (c) or S. aureus PGN (d). Results expressed as fold change relative to the control (WT tissues) were obtained and are presented as the mean ± SD of eight technical replicates. *p < 0.05, two-tailed t test (closed-testing procedure). The results shown are representative of two biological replicates.

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