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. 2016 Mar 2;7(11):11945–11958. doi: 10.18632/oncotarget.7858

Figure 3. TNF-α blockade and HUVECs replicative senescence and SASP acquisition.

Figure 3

A. Cumulative population doublings (CPDs) of HUVECs exposed to continuous anti-TNF-α treatment and of control cultures from 34 CPDs to complete growth arrest. Y axis, CPD; x axis, number of passages. B. Percentage of SA-β-Gal-positive cells at the beginning of the curve (young cells) and at its end (senescent cells), with/without anti-TNF-α treatment. C. p16/Ink4a mRNA expression in young and senescent cells with/without anti-TNF-α treatment. Data expressed as fold changes vs young cells. D. PAI1 mRNA expression in young and senescent cells with/without anti-TNF-α treatment. Data expressed as fold changes vs young cells. E. IL-6 release (pg/ml per 100,000 cells) into the culture medium by young and senescent cells with/without anti-TNF-α treatment. F. eNOS mRNA expression in young and senescent cells with/without anti-TNF-α treatment. Data expressed as fold changes vs young cells. G. MiR-146a-5p expression in young and senescent cells with/without anti-TNF-α treatment. Data expressed as fold changes vs young cells. H. MiR-126-3p expression in young and senescent cells with/without anti-TNF-α treatment. Data expressed as fold changes vs young cells. I. Irak1, Spred1 and IL1β expression and densitometry data (normalized to β-actin) in young and senescent cells with/without anti-TNF-α treatment. * Student's t test, p < 0.05. Data are mean ± S.D. of 3 independent experiments.

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