Figure 7.

Overexpression of ERα induces AMPK activation, autophagic signaling, and CHOP suppression. A, overexpression of HA-tagged ERα in Min6 β-cells increases AMPK protein and LC3B processing while reducing p62 and CHOP protein levels (n = 3/group in triplicate). B, ERα overexpression (ERα virus administration tested at four doses: 5, 10, 20, and 50 μl) promotes a dose-dependent reduction in CHOP protein (performed in triplicate). C, ERα overexpression (50 μl of virus administered) protects against H₂O₂-induced increase in CHOP protein (performed in triplicate; H₂O₂ 100 μm, PPT 100 nm, ICI 1 μm for 24 h). D, ERα-specific agonist PPT blunts H₂O₂-induced increase in CHOP protein, and this effect is blunted by the ERα antagonist ICI (performed in triplicate). E–G, PPT reduces Tg-induced phosphorylation of eIF2α and CHOP protein expression in Min6 β-cells (n = 3/condition in triplicate; Tg 500 nm for 18 h; and PPT 100 nm for 18 h). Values are mean ± S.E., *, p < 0.05, significant difference from control (Scr) cells or vehicle-treated cells; #, p < 0.5, significant difference from thapsigargin-treated cells. AU, arbitrary units.