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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2017 Jan 5;37(3):446–454. doi: 10.1161/ATVBAHA.116.308606

Figure 1. Olfm2 was upregulated in SMC phenotypic modulation both in vitro and in vivo.

Figure 1

A, PDGF-BB induced Olfm2 expression in primary RASMCs. Serum-starved RASMCs were treated with vehicle (−) or PDGF-BB (+, 20 ng/ml) for the time indicated. Western blotting was performed to examine the expression of Olfm2, SMC markers, and proliferation marker PCNA. B–E, Quantification of Olfm2, SMC markers and PCNA expression shown in A by normalizing to the TUBA1 level. *, P < 0.05 vs. vehicle-treated group (0 h) (n=3). F, Olfm2 expression was increased in rat carotid arteries after balloon injury (BI). Tissue lysates from uninjured (−) or balloon-injured (BI, +) carotid arteries with different days (d) were prepared for Western blotting analysis of Olfm2, SMC marker, and PCNA expression. G–J, Quantification of the protein expression shown in F by normalizing to the TUBA1 level. *, P < 0.05 vs. uninjured group (d 0) (n=3).