Figure 6.

Burning influences skin barrier, causes release of intracellular LDH and stress-related metabolic differences in OS-REp. (A) Transepithelial electrical resistance (TEER_{1000 Hz}) was measured with a custom-made system before (0 h) and at certain time points after burning. It revealed stagnation in TEER_{1000 Hz} values of burned models, while the control’s TEER_{1000 Hz} increased over cultivation time. (3 biological replicates in independent test runs with 4–12 technical replicates each; mean values ± SD; Kruskal-Wallis test with Dunn’s multiple comparisons test, * p < 0.05, ** p < 0.01, **** p < 0.0001 compared to the control. ° p < 0.05, °° p < 0.01 compared to burned models). (B) Glucose consumption subtracted by lactate production in mM. The glucose consumption is calculated in comparison to the glucose level measured in the fresh medium. Burning results in a significant lower ratio for the first three days after burning in comparison to the control, no matter the treatment. Glucose consumption and lactate production values can be found in the supplements (Supplementary Figure S5) (3 biological replicates in independent test runs with 3 technical replicates each; mean values ± SD; Kruskal-Wallis test with Dunn’s multiple comparisons test, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared to the control). (C) Burning leads to cellular disruption and a peak of lactate dehydrogenase (LDH) levels in the supernatant directly after injury but decreases after 24 h (3 biological replicates in independent test runs with 3 technical replicates each; mean values ± SD; Kruskal-Wallis test with Dunn’s multiple comparisons test, ** p < 0.01, *** p < 0.001, compared to the control).