Figure 4 | Scientific Reports

Figure 4

From: Proteomics-based functional studies reveal that galectin-3 plays a protective role in the pathogenesis of intestinal Behçet’s disease

Figure 4

Loss of galectin-3 activates endoplasmic reticulum (ER) stress and promotes cell death in HT-29 cells. (A,B) Expression of ER and cellular stress indicator proteins GRP78 and XBP1s in cells treated with LPS (A,B). Transcript levels were quantified by real-time quantitative reverse transcription polymerase chain reaction and normalized to β-actin expression levels. (C) Protein levels were quantified by western blotting and normalized to β-actin. *p < 0.05 vs. SCR, **p < 0.01 vs. SCR, ***p < 0.05 vs. SCR, #p < 0.05 vs. LPS, ###p < 0.005 vs. LPS. Veh, treated with phosphate-buffered saline; LPS, treated with lipopolysaccharide; rhGal3, treated with recombinant human galectin-3; SCR, scramble control HT-29 cell; shLGALS3, HT-29 cell expressing stably LGALS3 shRNA. (D) Effects of galectin-3 on cell death by ER stress inducer, LPS, were shown through Annexin V/PI staining. Data are presented as mean ± SD (n = 3). Veh, treated with phosphate-buffered saline; LPS treated with lipopolysaccharide; rhGal3, treated with recombinant human galectin-3 (10 μM); SCR, scramble control HT-29 cell; shLGALS3, HT-29 cell stably expressing LGALS3 shRNA.

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