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(A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. <t>ANOVA</t> with Fishers multiple comparisons test was performed <t>in</t> <t>Minitab</t> (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.
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(A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. <t>ANOVA</t> with Fishers multiple comparisons test was performed <t>in</t> <t>Minitab</t> (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.
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(A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. <t>ANOVA</t> with Fishers multiple comparisons test was performed <t>in</t> <t>Minitab</t> (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.
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(A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. <t>ANOVA</t> with Fishers multiple comparisons test was performed <t>in</t> <t>Minitab</t> (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.
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Image Search Results


(A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. ANOVA with Fishers multiple comparisons test was performed in Minitab (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.

Journal:

Article Title: The oxidative stress mediator 4-hydroxynonenal is an intracellular agonist of the nuclear receptor peroxisome proliferator-activated receptor-?/? (PPAR?/?)

doi: 10.1016/j.freeradbiomed.2007.01.003

Figure Lengend Snippet: (A) 4-HNE regulates gene expression in a PPARβ/δ-dependent manner. MuSH WT and MuSHβ/δ−/− cells were treated with 13(S)-HODE and 4-HNE overnight and the cells were lysed. Total RNA was extracted using Tri-Reagent and RT-PCR performed for ADRP and corrected for β-actin expression. N = 3. ANOVA with Fishers multiple comparisons test was performed in Minitab (State College, PA). Bars with different letters are significantly different (P<0.05). (B) PPARβ/δ is crucial in ameliorating the toxic effects of 4-HNE. MuSHWT and MuSHβ/δ−/− hepatocytes were treated with 0, 0.1, 0.3, 1, 3, 10 or 25 μM 4-HNE for 24 h. Hepatocytes treated with concentrations of 50 μM or higher 4-HNE do not survive, regardless of genotype. The data is normalized for % viable cells, shown on the y-axis. N = 8. Representative of six independent experiments. (C). PPARβ/δ−/− cells are more sensitive to arsenic induced toxicity. MuSHWT and MuSHβ/δ−/− hepatocytes were treated graded concentrations of sodium arsenite for 24 h. The data is normalized for % viable cells, shown on the y-axis. n = 5. Representative of two independent experiments. *P<0.05 compared with MuSH PPARβ/δ−/− hepatocytes. (D). Activation of PPARβ/δ leads to protection from oxidative damage. MuSHWT cells were pre-treated with vehicle or TTA (25 μM) for 6 h prior to treatment with 4-HNE. n= 5. *P<0.05 compared to vehicle-treated counterpart. (E). Inhibition of PPARβ/δ leads to increased susceptibility to oxidative damage. MuSHWT cells were pre-treated with vehicle or GW9662 (10 μM) for 6 h prior to treatment with 4-HNE. n = 5. *P<0.05 compared to vehicle-treated counterpart.

Article Snippet: ANOVA with Fishers multiple comparisons test was performed in Minitab (State College, PA).

Techniques: Gene Expression, Reverse Transcription Polymerase Chain Reaction, Expressing, Activation Assay, Inhibition