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. Author manuscript; available in PMC: 2018 Apr 1.
Published in final edited form as: Nat Med. 2017 Feb 20;23(4):429–438. doi: 10.1038/nm.4287

Figure 5. APOL1 risk variants induce inflammatory cell death (pyroptosis) in cells.

Figure 5

(a) Representative Western blot analysis of caspase3 (Casp3) and cleaved caspase3 (cCasp3) following transient transfection with TRE-APOL1-G0/G1/G2. UV exposure served as apoptosis positive control. n = 5. (b) Representative Western blot analysis of caspase1 (Casp1) and cleaved caspase1 (cCasp1) following transient transfection of TRE-APOL1-G0/G1/G2. GFP served as an APOL1 expression reference, α-tubulin as loading control and LPS as pyroptosis positive control. Western blot analysis of mature IL1β in medium from the same transfected HeLa cells. (c) Cell toxicity (measured by propidium iodide staining) in stably transfected TRE-GFP/APOL1-G1 HEK293 cells, with (APOL1) or without (CTL) doxycycline and in the presence of the indicated caspase1 inhibitors (concentration see Methods). Experiments were done in triplicates. Data are presented as means ± s.e.m, and Student’s t-test, P = 0.0015 (Ac-YVAD-CHO), 0.00018 (VX765) compared to APOL1. (d) Cell toxicity (measured by LDH release to the medium) in stably transfected TRE-GFP/APOL1-G1 HEK293 cells with (APOL1) or without (CTL) doxycycline and with indicated inhibitors (concentration see Methods). A representative experiment out of three is presented; each experiment was done in triplicates. All data are presented as means ± s.e.m, and Student’s t-test, P < 0.05.