Influence of Endogenous Cardiac Glycosides, Digoxin, and Marinobufagenin in the Physiology of Epithelial Cells

Figure 4

Participation of c-Src and ERK1/2 in the signaling pathway that leads to GJIC and TER increase by treatment with digoxin and marinobufagenin. (a, b) Pretreatment of monolayers of MDCK-W with inhibitors of c-Src (PP2, 10 μM) and ERK1/2 (PD98059, 25 μM) suppresses the enhancement of GJIC (a(I, II) and b(I, II)) and TER (a(III) and b(III)) induced by digoxin (a) or marinobufagenin (b) in MDCK cells in mature monolayers. (I, II) Effect of inhibitors on GJIC. (I) Series of representative images of dye transfer trial of each treatment assayed. (II) A bar chart comparing the average number of cells stained on each condition, as indicated below by each bar. The number of repeats is indicated in the upper part of each bar. Simple, paired comparisons (Student’s t) were made between treatment conditions, as indicated by the lines above bars. ; . (III) Bar charts comparing the mean ± SE (n = 9). Value of TER (Ohms·cm²) at different treatment conditions, as indicated in the inset, at 24, 48, and 72 hours of treatment ; of simple, pairwise comparisons (Student’s t) of TER values obtained from monolayers treated with digoxin or marinobufagenin in the presence or absence of PD or PP2.

(a)

(b)