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. 2016 Jul;186(7):1825–1836. doi: 10.1016/j.ajpath.2016.03.009

Figure 4.

Figure 4

Functional LEC features in AML cells with or without TSC2 correction support an LEC lineage derivation. A: Tubulogenesis assay reveals tubule formation by TSC2+ cells (arrows) but not by TSC2− cells when cultured in growth factor–depleted Matrigel in the presence of 10 ng/mL of vascular endothelial growth factor. B: TEER assays reveal higher transelectrical resistance in TSC2+ monolayers than in TSC2− monolayers. C: Dextran differential transport assays reveal TSC2+ cells higher permeability compared with TSC2− cells. D: The expression of several cytokine mRNAs is up-regulated by exposure to TLR ligands in both TSC2− and TSC2+ cells. However, the increases in mRNA levels are higher in TSC2+ cells. E: Proliferation assay showing decreased proliferation of TSC2− and TSC2+ cells after treatment with 10 nmol/L lymphangiogenesis inhibitor NCTD. Data are expressed as means ± SD. ∗P < 0.05, ∗∗P < 0.01, by t-test for the mean of the end point. Scale bar = 100 μm. AML, angiomyolipoma; FITC, fluorescein isothiocyanate; IFN, interferon; LEC, lymphatic endothelial cell; NCTD, norcantharidin; TEER, transepithelial electrical resistance; TLR, Toll-like receptor; TNF-α, tumor necrosis factor-α; TSC2, tuberous sclerosis complex-2; V, vehicle alone.