Fig. 2 | Scientific Reports

Fig. 2

From: Phenotype disruption of umbilical cord derived MSC by cyclic mechanical stretch and hyperoxia mediated by p21

Fig. 2Fig. 2

UC-MSC phenotype alterations by cyclic mechanical stretch (CMS) and hyperoxia (HOX). (A + B) Intracellular phenotype alterations in umbilical cord MSC (UCMSC) of newborn infants after exposure to CMS and/or HOX. (A) Western blot analysis showed reduced levels of PDGFRα after CMS and HOX 80% whereby HOX 80% and HOX 80% plus CMS demonstrated the largest effect size after 72 h treatment. n = 3 independent MSC cultures. (B) Western blot analysis showed no significant change in α-SMA expression after selective and combined treatment with CMS and HOX 80% for 72 h. n = 3 independent MSC cultures. The bar graphs show the densitometry results expressed as the ratio of adjusted total band volume normalized to ß-Actin and control. (C) CMS and/or HOX 80% increased cellular senescence–associated β-galactosidase (SA β-Gal) activity (blue; bright-field microscopy) after 72 h of exposure. Representative experiment of n = 4 independent MSC cultures. Scale bar 250 μm. Bar graph shows mean percentage change of β-Gal positive cells compared to unexposed UC-MSC. Data are expressed as box plot with median and interquartile range, *p < 0.05, **p < 0.01, by paired t-test, comparing exposures to the control situation. All full-length blots/gels from Figure 2 are presented in Supplementary Figure S1.

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