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. Author manuscript; available in PMC: 2012 Nov 22.
Published in final edited form as: J Am Coll Cardiol. 2011 Nov 22;58(22):2332–2339. doi: 10.1016/j.jacc.2011.07.048

Figure 4.

Figure 4

Function of gap junctions was assessed by modified scrape loading. Lucifer Yellow (LY; 400kDa) spreads extensively through myocytes from WT hearts (A), far beyond the spread of TRD (B; 10000kDa). Overlay image is seen in C. In the ACE8/8 hearts LY spread is decreased (D) with fewer cells coupled beyond the TRD (E). Overlay image indicates that fewer cells are coupled in these ACE8/8 hearts (F). Treatment of mice with PP1 restores normal dye spread (G) to well beyond the TRD (H). Note that the overlay image from WT mice (C) and from the PP1 treated mice (I) are similar in the extent of dye spread seen. Quantification of the overall dye spread shows that the overall dye spread in the ACE8/8 mice is significantly decreased (0.14±0.01 mm vs. 0.21±0.02 mm respectively, P < 0.05) and that is restored to the normal level after PP1 treatment (0.21±0.02 mm in WT vs. 0.20±0.02 mm in PP1, P = NS, PP1 vs. ACE8/8 P < 0.05). Analysis of the anisotropy of dye spread indicates that in this model dye spread is lost in both the transverse and longitudinal directions, although more prominent in the longitudinal direction (K). Treatment of wild-type mice with PP1 did not significantly change the gap junction conduction (P = NS) (n=5 for all groups).