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. Author manuscript; available in PMC: 2014 Aug 6.
Published in final edited form as: Circulation. 2013 Jul 9;128(6):632–642. doi: 10.1161/CIRCULATIONAHA.113.002714

Figure 2.

Figure 2

OS Induces NLRP3 Inflammasomes in ECs via SREBP2. (A) Representative immunoblot for pro-caspase-1, caspase-1 p20, pro-IL-1β, and IL-1β p17 in HUVECs exposed to PS or OS for 14 hr and (B) in HUVECs treated with Adenovirus-null (Ad-null, 5 MOI), Adenovirus-SREBP2(N) tagged with HA [Ad-SREBP2(N), 2.5 MOI or 5 MOI]. (C) Caspase-1 activity of extracts from HUVECs treated with Ad-null, 5 MOI, Ad-SREBP2(N), 2.5 MOI or 5 MOI. Data are mean ± SEM normalized to Ad-null group for each independent experiment. Mann-Whitney U test with exact method was used. *p < 0.05 compared with Ad-null. (D) Representative immunoblot of pro-caspase-1, caspase-1 p20, pro-IL-1β, IL-1β p17, SREBP2 precursor, and mature form of SREBP2 in HUVECs transfected with 20 nM control RNA or SREBP2 siRNA for 48 hr, then exposed to static conditions or OS for 14 hr. (E) Representative immunoblot for pro-caspase-1, caspase-1 p20, pro-IL-1β, IL-1β p17, and NLPR3 in HUVECs transfected with 20 nM control RNA or NLRP3 siRNA for 48 hr, then exposed to static conditions or OS for 14 hr. (F) Representative immunoblot of pro-caspase-1, caspase-1 p20, pro-IL-1β, IL-1β p17, and ASC in HUVECs transfected with 20 nM control RNA or ASC siRNA for 48 hr, then exposed to static conditions or OS for 14 hr.