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. Author manuscript; available in PMC: 2014 May 27.
Published in final edited form as: Cell Rep. 2014 Apr 13;7(2):412–423. doi: 10.1016/j.celrep.2014.03.025

Figure 6. Increased Flcn-null epithelial cell apoptosis is rescued by AICAR and constitutively active AMPK.

Figure 6

(A) Flcn knockdown downregulates membrane localization of E-cadherin (red). Scale bars, 25 μM.

See also Figure S5 and S6.

(B) Flcn knockdown decreases trans-epithelial resistance (TER). TER of siContr-transfected NMuMG cells was taken as 100%.

(C) Cleaved caspase-3 is upregulated by siFlcn.

(D) Flcn knockdown induces DNA fragmentation (TUNEL assay) of NMuMG cells.

(E) AICAR and constitutively active AMPK (AMPK-CA) rescue disruption of epithelial cell morphology caused by siFlcn. Cells were treated either with 100 mM AICAR or diluent, or were infected with AdAMPK-CA or control adenovirus. Scale bars, 100 μM.

(F–G) Expression of AMPK-CA (F) and AICAR-induced AMPK and ACC (G) phosphorylation in epithelial NMuMG cells.

(H–I) DNA fragmentation (H) and epithelial cell death (I) induced by Flcn loss is rescued by AICAR and AMPK-CA. Data represent percentage of TUNEL-positive (H) or dead (I) cells per total number of cells taken as 100%.

Data are mean ± SE, n=3.