AI Article Synopsis
- PPARs are found in bovine uterus and are influenced by arachidonic acid metabolites, which play a role in regulating apoptosis in endometrial stromal cells (ESC).
- Silencing PPARα and PPARδ genes leads to increased DNA fragmentation and higher levels of caspase-3 and caspase-8, indicating more apoptosis, whereas silencing PPARγ does not significantly change apoptosis levels.
- The study suggests that PPARα and PPARδ inhibit apoptosis in bovine ESC, and that arachidonic acid metabolites affect this process.
Article Abstract
Peroxisome proliferator-activated receptors (PPARs) are expressed in bovine uterus, and their agonists are arachidonic acid (AA) metabolites. We hypothesised that silencing of PPAR genes in bovine endometrial stromal cells (ESC) would change the intracellular signalling through PPAR and affect apoptosis after cell treatment with different AA metabolites. The study's aims are detection of apoptosis and examining the influence of prostaglandins and leukotrienes on apoptosis occurring in physiological ESC and cells with silenced PPAR (α, δ, and γ) genes. Silencing the PPARα and PPARδ genes in cells resulted in increased DNA fragmentation and mRNA and protein expression of caspase (CASP) -3 and -8 (P < 0.05). Neither DNA fragmentation nor the mRNA and protein expression of CASP3 and -8 in cells with silenced PPARγ gene were changed compared to physiological cells (P > 0.05). Among PPARs, PPARα and PPARδ appear to inhibit apoptosis, and AA metabolites, as PPAR agonists, modify this process in bovine ESC.
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| http://dx.doi.org/10.1016/j.prostaglandins.2019.106336 | DOI Listing |
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