Fig. 6

The inhibition of Aurora A and Erk1/2 increases the level of stemness-associated genes including SOX2, OCT4, and NANOG and modulates the STAT3-AKT/GSK3β signaling in obese ASCs. a, b The gene levels of genes associated with pluripotency (SOX2, OCT4, NANOG, and KLF4). The data are based on four experiments and presented as mean ± SEM. Student’s t test was used. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. c Western blot analyses of pSTAT3, STAT3, pAKT, AKT, pGSK3β, GSK3β, pErk1/2, Erk1/2, and β-actin. The intensity of proteins was normalized to β-actin, and ratios were quantified with image J. Lean ASCvis were set as 1. d The gene levels of SOX2, OCT4, and NANOG in obese ASCs untreated or treated with a GSK3β inhibitor (CHIR99021, 2 μM) for 48 h. The data are based on three experiments and presented as mean ± SEM. Student’s t test was used. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. e Schematic illustration of the proposed working model. Obese ASCs with shortened primary cilia, which render these cells dysfunctional, can be partly rescued by treatment with low dose of Aurora A or Erk1/2 inhibitors. This improves their stemness, motility, and differentiation capacity and modifies their cytokine secretion