Effect of pioglitazone treatment on endoplasmic reticulum stress response in human adipose and in palmitate-induced stress in human liver and adipose cell lines
Am J Physiol Endocrinol Metab Das et al.
295: E393
Figure S1 -
Expression of ER stress response transcripts before and after pioglitazone in adipose tissue from obese individuals. A) Data from 20 human volunteers are shown as a line graph, with each individual represented by a different color. ER stress genes were normalized to 18S RNA. Pre-treatment values for each gene are shown on the left, with post-treatment (labeled with P) on right. B) XBP1 expression before and after treatment; -, negative control (untreated HepG2 cells); +, positive control (HepG2 cells treated with tunicamycin); Pre, before pioglitazone therapy; Post, after pioglitazone therapy. Samples from three representative human volunteers are shown.
Figure S2 -
Pioglitazone does not induce ER stress in HepG2 cells. A) Expression of ER stress transcripts after 16 hours of pretreatment of pioglitaozne or DMSO, followed by 12 h of treatment with BSA (control) in presence or absence of pioglitazone. Values were normalized to 18S RNA, then ratios were normalized to the mean value of control (DMSO) condition as 1. Data are expressed as mean ± SD of three independent experiments with two biological replicates. B) XBP1 splicing for the experiment in 2S A.
Figure S3 -
Pretreatment of pioglitazone does not inhibit palmitate induced ER stress in SGBS cells. A) Expression of ER stress response transcripts after 16 h pretreatment of SGBS cells with either pioglitaozne or control (DMSO), followed by 12 h treatment with palmitate (0.5 mM) or control (BSA). Expression data were first normalized to 18S RNA, then scaled to the lowest value of the control sample as 1 for each condition. Data shown are representative of one experiment. B) XBP1 splicing for the experiment described in A.