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Fig. 3 | Lipids in Health and Disease

Fig. 3

From: GRP78/BiP alleviates oxLDL-induced hepatotoxicity in familial hypercholesterolemia caused by missense variants of LDLR in a HepG2 cellular model

Fig. 3

A-B Effect of oxLDL on UPR in HepG2 cells stably expressing WT /variants of LDLR A Western blots showing the expression pattern of ER chaperone-BiP (vi) and ER stress sensors (iii-v and vii-ix), apoptotic and inflammatory markers (xi-xvii) after 24 h of oxLDL treatment. NTC-Non treated control, TM-Tunicamycin (2 µg per ml, 24 h), DMSO-vehicle control, oxLDL-oxidized LDL (100 µg per ml, 24 h). GAPDH and Alpha tubulin were used as loading controls. Image panels were created using the QuickFigures plugin of ImageJ software, the contrast was enhanced uniformly, and confirmed that there were no significant changes with respect to proteins that exhibited minimal basal expression. ‘**’ represents the intermediate isoforms of ATF6. B (i-xi))-Histograms representing the change in expression of all the target proteins evaluated. For each of the four types of HepG2 cells studied (HepG2mock, HepG2WT−LDLR, HepG2D482H−LDLR, and HepG2C667F−LDLR), comparisons and statistical analyses were carried out between the respective non-treated versus treated conditions and represented as mean + SD. Statistical analyses were carried out using Dunnett’s 1-way ANOVA, or 2-way ANOVA for ATF6 (Turkey’s post hoc test), where P < 0.05 = *, P < 0. 01 = **, P < 0.001 = ***, P < 0.0001 = ****, ns = not significant, n = 3 replicates

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