Involvement of PPAR-γ and p53 in DHA-induced apoptosis in Reh cells
Molecular and Cellular Biochemistry, ISSN: 0300-8177, Vol: 304, Issue: 1-2, Page: 71-77
2007
- 44Citations
- 21Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations44
- Citation Indexes44
- 44
- CrossRef33
- Captures21
- Readers21
- 21
Article Description
Docosahexaenoeic acid (DHA, 22:6 n-3) is an omega-3 polyunsaturated fatty acid that is found in fish oil and exerts cytotoxic effect on a variety of cell lines. The molecular target, responsible for mediating this effect of DHA, still remains unknown. In this report, we presented experimental evidences for the role of PPAR-γ in conveying the cytotoxic effect of DHA. We showed that DHA induces apoptosis in Reh and Ramos cells and apoptotic effect of DHA is inhibited by the PPAR-γ antagonist GW9662, indicating that PPAR-γ functions as the mediator of the apoptotic effect of DHA. Furthermore, our result showed that DHA induces the PPAR-γ protein levels in both Reh and Ramos cells. Interestingly, DHA was found to induce the expression of p53 protein in Reh cells in a PPAR-γ-dependent manner. The up-regulation of p53 protein by DHA kinetically correlated with the activation of caspase 9, caspase 3, and induction of apoptosis, suggesting a role for p53 in DHA-mediated apoptosis in Reh cells. Taken together, these findings suggest a new signaling pathway, DHA-PPAR-γ-p53, in mediating the apoptotic effect of DHA in Reh cells. © Springer Science+Business Media, LLC 2007.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34748848017&origin=inward; http://dx.doi.org/10.1007/s11010-007-9487-5; http://www.ncbi.nlm.nih.gov/pubmed/17487454; http://link.springer.com/10.1007/s11010-007-9487-5; https://dx.doi.org/10.1007/s11010-007-9487-5; https://link.springer.com/article/10.1007/s11010-007-9487-5; http://www.springerlink.com/index/10.1007/s11010-007-9487-5; http://www.springerlink.com/index/pdf/10.1007/s11010-007-9487-5
Springer Science and Business Media LLC
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