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. 2017 Dec 15;5(3):273–288. doi: 10.1016/j.jcmgh.2017.11.015

Figure 3.

Figure 3

N-WASP depletion leads to junction abnormalities and increased permeability in vitro. (A) Western blot showing >90% knockdown of N-WASP using N-WASP–specific shRNA. (B) NWKD cells polarized normally and showed apical microvilli marked by phalloidin (left) and well-defined junction complexes marked by E-cadherin (right). (C) Immunolocalization of junction proteins showed normal patterns of E-cadherin (top) and ZO-1 (middle), while occludin (bottom) was less concentrated at cell junctions and displayed more cytoplasmic staining in NWKD cells. (D) In both WT and NWKD monolayers, E-cadherin and ZO-1 pixel density was tightly focused at the AJC, with very little cytoplasmic signal; occludin pixel intensity was less concentrated at intercellular junctions in NWKD monolayers. (E) NWKD monolayers developed TER more quickly (†) during the first 14 days, but had an overall lower maximal steady-state TER compared with WT monolayers (‡P < .05). (B and C) Scale bars: 5 μm.