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. Author manuscript; available in PMC: 2018 Apr 1.
Published in final edited form as: Small. 2017 Feb 17;13(15):10.1002/smll.201603737. doi: 10.1002/smll.201603737

Figure 6. Exacerbated response to biomechanical strain in HGPS iPS-SMCs is rescued by lovastatin and lonafarnib.

Figure 6

Relative mRNA expression levels of healthy and HGPS iPS-SMCs cultured under 0%, 9%, and 16% biomechanical strains for 24 hours. Injury marker (A) CAV1 and inflammation markers (B) IL6, (C) IL1B, and (D) JUN (* P<0.01 against 0% healthy iPS-SMCs, and # indicates P<0.01 against 0% HGPS iPS-SMCs; bars represent mean ± SD of n=5). DNA damage was evaluated in HGPS iPS-SMCs with H2A.X immunostaining (E) and quantified (F) (mean ± SD of n=3; **, P=0.0039). Senescence was measured in HGPS iPS-SMCs via β-galactosidase activity staining (G) and quantified (H) (mean ± SD of n=3; ns, not significant [P=0.0532]). Treatment of HGPS iPS-SMCs under 16% mechanical strain with lovastatin or lonafarnib prevented increased injury and inflammatory markers (I–L), while static control on a Petri dish failed to trigger a response [(§§, P<0.001; §, P=0.04; compared to no drug treatment; bars for lonafarnib and lovastatin represent mean ± SD of n=4; bars for static control represent mean ± SD of n=3].