Fig. 4 | Scientific Reports

Fig. 4

From: Retarding human adipose-derived MSCs senescence and promoting tendon repair using cell sheet engineering with a histone methyltransferase inhibitor

Fig. 4

Suppression of histone methyltransferase SETD7 enhanced differentiation capacity of hAD-MSCsin vitro. (A, B) Clonogenic activity and quantitative analysis of hAD-MSCs in earlier and senescent cultures with or without PFI-2 treatment. (C) Representative images of oil red staining in different passage of hAD-MSCs (P4 and P8) under induction condition with or without PFI-2 treatment, n = 3. Scale bar = 100 μm. (D) Alcian blue staining of hAD-MSCs in earlier and senescent under induction condition with or without FPI-2 treatment. (E, F) Alizarin red staining (F) and quantitative analysis (E) of earlier and senescent hAD-MSCs under induction condition with or without PFI-2 treatment, n = 3. Scale bar = 100 μm. (G, H) qRT-PCR (H) and western blot (G) analysis of tendon-associated genes and proteins in cell sheets from hAD-MSCs at P8, n = 3. Data shown from representative sample and represented as mean ± SD. Two-tailed Student’s test, *p < 0.05, **p < 0.01. Abbreviation: P, passage. hAD-MSCs used for cell sheets induction were at P8.

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