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. Author manuscript; available in PMC: 2020 Apr 23.
Published in final edited form as: Cell Rep. 2020 Feb 18;30(7):2209–2224.e5. doi: 10.1016/j.celrep.2020.01.064

Figure 1. Oxidative Stress-Induced TLR2 Activation Induces AP Complement Factor Expression.

Figure 1.

(A–D) qPCR of CFB (A and C) and C3 (B and D) expression in BMDMs or THP1s treated with 20 nM of Pam3Cys4.

(E–I) IHC of C3d (purple) in healthy non-disease donor (E and F) and AMD donor eyes (G–I).

(J and K) Black arrow and black asterisk denote C3d in CC and basal laminar deposits in AMD donor eye (representative of n = 4 non-disease donor eyes, n = 5 AMD donor eyes). qPCR of CFB (J) and C3 (K) in ARPE-19 cells treated with 20 nm of Pam3Cys4. Data shown are mean ± SD for a representative of three separate experiments. CC, choriocapillaris; RPE, retinal pigment epithelium; BM, Bruch’s membrane.

(L) Generation and chemical structure of CEP-adduct from DHA.

(M and N) qPCR of (M) C3 and (N) CFB in hfRPE cells treated with 0.1 µg of IgG or anti-TLR2 antibody prior to 10 µM of CEP-HSA for 24 h.

(O) IHC of TLR2 (purple) in a healthy donor. Bottom panel (black box) is photobleached to illustrate apical and basolateral RPE immunoreactivity (n = 4 non-disease donor eyes).

(P) Secreted CFB at 24 h and C3 at 48 h in hfRPE cells treated with 17.5 µM or 35 µM of CEP-HSA and 20 nM of Pam3Cys4, mean ± SD representative of three independent experiments: *p < 0.05; **p < 0.01; ***p < 0.001.

See also Figures S1 and S2.