Fig 2: FKBP11 and GRP78 expression levels are increased in TNBS-induced colitis. Western blot analyses revealed that the expression levels of (A) FKBP11 and GRP78, and (B) active caspase-3 in TNBS induced colitis are significantly enhanced 3 days post-treatment compared with the ETOH group. Bar graphs demonstrate the quantitative analysis of FKBP11, GRP78 and active caspase-3 vs. GAPDH. (C) Immunohistochemistry analysis of FKBP11 and GRP78 expression in colonic mucosa of mice treated with TNBS for 3 days (scale bar, 50 µm). Data are presented as mean ± standard error (n=3). *P<0.05 vs. ETOH. ETOH, ethanol; TNBS, 2, 4, 6-trinitrobenzenesulphonic acid; FKBP11, FK506 binding protein 11; GRP78, 78 kDa glucose-regulated protein.

Fig 3: Twist knockdown induces cell death in CisR OC cells. (A) The relative cell viability. (B) Western blot analysis for anti-apoptotic protein, Bcl-2 and apoptotic proteins, Bax, cleaved caspase-9 and cleaved caspase-3. (C) Tunicamycin-induced ER stress response in CisR cells assayed by Western blot analysis of GRP78, cleaved ATF-6 and CHOP. Parental: non-transfected parental cells; siNC: cisplatin resistance cells transfected with non-targeting negative control siRNA; siTwist: cisplatin resistance cells transfected with Twist siRNA. Values were represented as mean ± SD. # p < 0.05, compared with the parental group, * p < 0.05, compared with siNC group and † p < 0.05, compared with 0 h of CisR group.

Fig 4: Twist knockdown reduces cell growth potential in CisR OC cells. (A) Western blot analysis for DNA repair proteins, PARP1 and XRCC1. (B) The cell survival analysis assayed by clonogenic assay. (C) Western blot analysis for expression of ER stress signaling proteins, GRP78, cleaved ATF-6 and CHOP. Parental: non-transfected parental cells; siNC: cisplatin resistance cells transfected with non-targeting negative control siRNA; siTwist: cisplatin resistance cells transfected with Twist siRNA. Values were represented as mean ± SD. # p < 0.05, compared with the parental group and * p < 0.05, compared with siNC group.

Fig 5: PKA signaling pathway is involved in the effects of IMD on SERCA activity and endoplasmic reticulum stress. Cardiomyocytes were treated with TG in the presence or absence of 100 nM IMD or 10 µM PKA inhibitor H-89 for 24 h. (A) SERCA activity. (B) Representative western blot images of p-PLB, t-PLB, SERCA2, GRP78, CHOP and caspase-12. Semi-quantification of (C) p-PLB/t-PLB, (D) SERCA2, (E) GRP78, (F) CHOP and (G) caspase-12 protein levels. Data were analyzed with a student's t-test for two group comparison. Data are presented as the mean ± SD. n=3. *P<0.05 and **P<0.01. IMD, intermedin; SERCA, sarco/endoplasmic reticulum calcium ATPase; PLB, phospholamban; p-, phosphorylated; t-, total; GRP78, 78 kDa glucose-regulated protein; CHOP, C/EBP-homologous protein; PKA, protein kinase A; TG, thapsigargin; nmol Pi/mg prot/min, nanomoles of phosphorus ions per milligram of protein per minute.