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The role of PPARγ in TBBPA-mediated endocrine disrupting effects in human choriocarcinoma JEG-3 cells.

Honkisz E, Wójtowicz AK - Mol. Cell. Biochem. (2015)

Bottom Line: Our results showed that after TBBPA treatment at 10 nM and 10 µM, PPARγ protein expression increased in a time-dependent manner until 48 h and then slightly decreased at 72 h but was still above the control level.Finally, in the present study, we demonstrated that TBBPA at all of the tested doses significantly increased caspase-3 activity compared with that of the vehicle control.These results showed the up-regulation of PPARγ protein expression after TBBPA exposure in human placental cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Animal Biotechnology, University of Agriculture, Rędzina 1B, 30-248, Kraków, Poland.

ABSTRACT
The goal of the present study was to investigate the action of TBBPA on PPARγ protein expression in vitro in human choriocarcinoma-derived placental JEG-3 cells. We also analyzed TBBPA for its action on placental secretion of progesterone and β-hCG, cell viability, and apoptosis. Our results showed that after TBBPA treatment at 10 nM and 10 µM, PPARγ protein expression increased in a time-dependent manner until 48 h and then slightly decreased at 72 h but was still above the control level. This alteration in PPARγ protein expression was accompanied by a decreased β-hCG level. Interestingly, co-treatment with the PPARγ antagonist GW9662 reversed the TBBPA-mediated changes in PPARγ protein expression but, according to β-hCG secretion, potentiated an inhibitory effect of TBBPA. Additionally, in our study, we assessed the ability of TBBPA to increase progesterone levels in JEG-3 cells compared with those of controls. Finally, in the present study, we demonstrated that TBBPA at all of the tested doses significantly increased caspase-3 activity compared with that of the vehicle control. The apoptotic action of TBBPA was also confirmed by Hoechst 33342 staining. These results showed the up-regulation of PPARγ protein expression after TBBPA exposure in human placental cells. Although co-treatment with antagonist of PPARγ reversed the TBBPA-mediated increase in this protein expression and restored it to the control level, it did not reverse the effect on β-hCG secretion. This indicated that the mechanism of TBBPA-induced changes in β-hCG secretion is PPARγ-independent.

No MeSH data available.


Related in: MedlinePlus

The effect of TBBPA (10 nM) in the presence of PPARγ agonist GW1929 and antagonist GW9662 on β-hCG secretion in JEG-3 cells after 48 h of exposure. Each point represents the mean ± SEM of two independent experiments, each of which consisted of ten replicates per treatment group. Data indicated with ***p < 0.001 reflects statistically significant differences relative to the control. Data indicated with ###p < 0.001 reflects statistically significant differences relative to TBBPA
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Fig5: The effect of TBBPA (10 nM) in the presence of PPARγ agonist GW1929 and antagonist GW9662 on β-hCG secretion in JEG-3 cells after 48 h of exposure. Each point represents the mean ± SEM of two independent experiments, each of which consisted of ten replicates per treatment group. Data indicated with ***p < 0.001 reflects statistically significant differences relative to the control. Data indicated with ###p < 0.001 reflects statistically significant differences relative to TBBPA

Mentions: 48 h of treatment with TBBPA at concentrations of 10 nM caused significant decreases in the β-hCG production of approximately 31 %, compared with that of the vehicle control (Fig. 5). However, after this time, co-treatment with antagonist did not restore the TBBPA-mediated decrease in the β-hCG level. In contrast, co-treatment with antagonist and TBBPA led to a 1.9-fold decrease in β-hCG production compared with that of TBBPA treatment alone. Interestingly, treatment with antagonist alone caused a 1.5-fold decrease in β-hCG secretion compared with that found upon TBBPA treatment. Treatment with agonist also reduced β-hCG secretion, but the effect was much greater and resulted in a significant decrease that was approximately 2.3-fold higher than that of the TBBPA treatment. Agonist as well as TBBPA reduced β-hCG release, but both exhibited synergy with co-treatment.Fig. 5


The role of PPARγ in TBBPA-mediated endocrine disrupting effects in human choriocarcinoma JEG-3 cells.

Honkisz E, Wójtowicz AK - Mol. Cell. Biochem. (2015)

The effect of TBBPA (10 nM) in the presence of PPARγ agonist GW1929 and antagonist GW9662 on β-hCG secretion in JEG-3 cells after 48 h of exposure. Each point represents the mean ± SEM of two independent experiments, each of which consisted of ten replicates per treatment group. Data indicated with ***p < 0.001 reflects statistically significant differences relative to the control. Data indicated with ###p < 0.001 reflects statistically significant differences relative to TBBPA
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4589557&req=5

Fig5: The effect of TBBPA (10 nM) in the presence of PPARγ agonist GW1929 and antagonist GW9662 on β-hCG secretion in JEG-3 cells after 48 h of exposure. Each point represents the mean ± SEM of two independent experiments, each of which consisted of ten replicates per treatment group. Data indicated with ***p < 0.001 reflects statistically significant differences relative to the control. Data indicated with ###p < 0.001 reflects statistically significant differences relative to TBBPA
Mentions: 48 h of treatment with TBBPA at concentrations of 10 nM caused significant decreases in the β-hCG production of approximately 31 %, compared with that of the vehicle control (Fig. 5). However, after this time, co-treatment with antagonist did not restore the TBBPA-mediated decrease in the β-hCG level. In contrast, co-treatment with antagonist and TBBPA led to a 1.9-fold decrease in β-hCG production compared with that of TBBPA treatment alone. Interestingly, treatment with antagonist alone caused a 1.5-fold decrease in β-hCG secretion compared with that found upon TBBPA treatment. Treatment with agonist also reduced β-hCG secretion, but the effect was much greater and resulted in a significant decrease that was approximately 2.3-fold higher than that of the TBBPA treatment. Agonist as well as TBBPA reduced β-hCG release, but both exhibited synergy with co-treatment.Fig. 5

Bottom Line: Our results showed that after TBBPA treatment at 10 nM and 10 µM, PPARγ protein expression increased in a time-dependent manner until 48 h and then slightly decreased at 72 h but was still above the control level.Finally, in the present study, we demonstrated that TBBPA at all of the tested doses significantly increased caspase-3 activity compared with that of the vehicle control.These results showed the up-regulation of PPARγ protein expression after TBBPA exposure in human placental cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Animal Biotechnology, University of Agriculture, Rędzina 1B, 30-248, Kraków, Poland.

ABSTRACT
The goal of the present study was to investigate the action of TBBPA on PPARγ protein expression in vitro in human choriocarcinoma-derived placental JEG-3 cells. We also analyzed TBBPA for its action on placental secretion of progesterone and β-hCG, cell viability, and apoptosis. Our results showed that after TBBPA treatment at 10 nM and 10 µM, PPARγ protein expression increased in a time-dependent manner until 48 h and then slightly decreased at 72 h but was still above the control level. This alteration in PPARγ protein expression was accompanied by a decreased β-hCG level. Interestingly, co-treatment with the PPARγ antagonist GW9662 reversed the TBBPA-mediated changes in PPARγ protein expression but, according to β-hCG secretion, potentiated an inhibitory effect of TBBPA. Additionally, in our study, we assessed the ability of TBBPA to increase progesterone levels in JEG-3 cells compared with those of controls. Finally, in the present study, we demonstrated that TBBPA at all of the tested doses significantly increased caspase-3 activity compared with that of the vehicle control. The apoptotic action of TBBPA was also confirmed by Hoechst 33342 staining. These results showed the up-regulation of PPARγ protein expression after TBBPA exposure in human placental cells. Although co-treatment with antagonist of PPARγ reversed the TBBPA-mediated increase in this protein expression and restored it to the control level, it did not reverse the effect on β-hCG secretion. This indicated that the mechanism of TBBPA-induced changes in β-hCG secretion is PPARγ-independent.

No MeSH data available.


Related in: MedlinePlus