Skip to main content
. Author manuscript; available in PMC: 2020 Feb 7.
Published in final edited form as: Cell Stem Cell. 2019 Jan 10;24(2):299–308.e6. doi: 10.1016/j.stem.2018.11.018

Figure 4. Genetic variants determine and predict individual differences in rosi responsiveness.

Figure 4.

(A) Sanger sequencing validation of the correction of A/A allele to C/C allele.

(B and C) PPARγ (B) and NFI (C) ChIP-qPCR for ABCA1, PDK4, ALAS2, and INS2 in SGBS WT and SGBS A>C adipocytes.

(D) mRNA expression of ABCA1 in SGBS WT and SGBS A>C adipocytes treated with DMSO, 1μM rosi or 10μM T091317 (n=3).

(E) mRNA expression of ABCA1 in hASC-derived adipocytes from 25 patients. Red dots represent patients P1-P5. Data are expressed as mean ± SEM of Rosi/DMSO fold change.

(F) Cholesterol efflux to serum in 3 patient-adipocytes carrying A/A and 3 patient-adipocytes carrying C/C treated with DMSO, 1μM rosi or 10μM T091317 (n=3).

(G and H) The change of total cholesterol (G) and LDL (H) levels after rosi treatment in patients carrying different rs4743771 genotypes.

RT-qPCR, ChIP-qPCR data are expressed as mean ± SEM. (*) p < 0.05, (**) p < 0.01, (***) p < 0.001, (ns) p > 0.05 in Student’s t-test.

See also Figure S4.