Fig. 2: Characterization of primed vs. naïve DhiPSC. | Nature Communications

Fig. 2: Characterization of primed vs. naïve DhiPSC.

From: Vascular progenitors generated from tankyrase inhibitor-regulated naïve diabetic human iPSC potentiate efficient revascularization of ischemic retina

Fig. 2

a IF stains of N-DhiPSC (line E1C1) for general pluripotency factors (TRA-1-81, NANOG) and naïve pluripotency proteins (NR5A2, STELLA/DPPA3, E-CADHERIN; Scale Bar = 50 μm). b Primed (P) vs. naïve (N) phosphorylated-STAT3 (P-STAT3) expression. Western blots were performed of isogenic P vs. N lysates of (left panel) three independent DhiPSC lines (E1C1, E1CA1, E1CA2), or (right panel) two independent non-diabetic fibroblast-hiPSC lines (C1.2, C2). ACTIN and total STAT3 (T-STAT3) served as internal loading controls. c Naïve-specific protein expression of TFAP2C31 in DhiPSC (E1C1) in P vs. N conditions. d Isogenic teratoma organoid quantifications from DhiPSC (E1C1) cultured in primed (blue bar) vs. naïve (red bar) conditions. Shown are quantifications per cross section of mesodermal (NG2+ chondroblast), definitive endodermal (CK8+ gut/glandular cells), and ectodermal (SOX2+ neural rosettes; retinal pigmented epithelium) structures from H&E stained slides. **p < 0.01; ***p < 0.001 (Mann-Whitney tests). e Western blots of XAV939-inhibited proteolysis of tankyrases 1 and 2 (TANK ½) and AXIN-1 proteins in isogenic primed vs. naïve conditions from DhiPSC (E1C1), and non-diabetic hiPSC (E5C3) and hESC (H9).

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