Omega-3 Fatty Acids Inhibit Endoplasmic Reticulum (ER) Stress in Human Coronary Artery Endothelial Cells

Figure 1

The effect of DHA on UPR marker expression and activation. HCAECs were treated with the solvent DMSO, 1.0 μM tunicamycin (TM), 1.0 μM DHA, or tunicamycin plus DHA (1.0 μM each) (TM/DHA) for 24 hours and protein extracts were prepared. Representative blots are shown in panel A and quantified in panel B through H phospho-IRE1α (b), IRE1α (c), phospho-PERK (d), PERK (e), ATF6 (f), GRP78 (g), and tubulin (h) expression were measured by Western blot. TM increased phospho-IRE1α and phospho-PERK levels and increased ATF6 and GRP78 expression, while treatment with DHA had no effect. In cells treated with TM and DHA, phospho-IRE1α and phospho-PERK levels decreased and ATF6 and GRP78 expression decreased relative to TM-treated cells. IRE1α, PERK, and tubulin expression did not change with any treatment. (a) Phospho-IRE1α. N = 6; and , respectively, relative to control cells; ^† and , respectively, relative to TM-treated cells. (b) IRE1α; N = 6. (c) Phospho-PERK; N = 6; and , respectively, relative to control cells. ^† relative to TM-treated cells. (d) PERK; N = 6. (e) ATF6; N = 6; and , respectively, relative to control cells. ^† and , respectively, relative to TM-treated cells. (f) GRP78; N = 6; and , respectively, relative to control cells. ^† relative to TM-treated cells. (g) Tubulin; N = 6.

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