ArticleBiology of reproduction2019
Rosiglitazone augments antioxidant response in the human trophoblast and prevents apoptosis†.
Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- CGKRK-targeted lipid nanoparticles enhanceiScience · 2025Article
- Rosiglitazone-Mediated Activation of PPARγ Induces PlGF Expression in Trophoblast Cells.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- Rosiglitazone-Mediated Activation of PPARγ Restores HO1 Expression in the Human Preeclamptic Placenta.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Antidiabetic Drugs Can Reduce the Harmful Impact of Chronic Smoking on Post-Traumatic Brain Injuries.International journal of molecular sciences · 2023Article
- Review
- The Potential for Placental Activation of PPARγ to Improve the Angiogenic Profile in Preeclampsia.Cells · 2022Article
- Candesartan Does Not Activate PPARγ and Its Target Genes in Early Gestation Trophoblasts.International journal of molecular sciences · 2022Article
- Mitochondrial Dysfunction in the Pathogenesis of Preeclampsia.Current hypertension reports · 2022Review
- Trophoblast Cell Subtypes and Dysfunction in the Placenta of Individuals with Preeclampsia Revealed by Single‑Cell RNA Sequencing.Molecules and cells · 2022Article
- PFOS Inhibited Normal Functional Development of Placenta Cells viaBiomedicines · 2021Article
- Maternal RND3/RhoE deficiency impairs placental mitochondrial function in preeclampsia by modulating the PPARγ-UCP2 cascade.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications.Antioxidants (Basel, Switzerland) · 2021Review
- Nobiletin, a hexamethoxyflavonoid from citrus pomace, attenuates G1 cell cycle arrest and apoptosis in hypoxia-induced human trophoblast cells of JEG-3 and BeWo via regulating the p53 signaling pathway.Food & nutrition research · 2021Article
- The Effects of 5,6,7,8,3',4'-Hexamethoxyflavone on Apoptosis of Cultured Human Choriocarcinoma Trophoblast Cells.Molecules (Basel, Switzerland) · 2020Article
- Comparative Study of PPARPPAR research · 2020Article
- QUEST MRI assessment of fetal brain oxidative stress in utero.NeuroImage · 2019Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Insufficient perfusion of the trophoblast by maternal blood is associated with an increased generation of reactive oxygen species and complications of the placenta. In this study, we first examined whether rosiglitazone, an agonist of the peroxisome proliferator-activated receptor-γ (PPARγ), protects the human trophoblast from oxidative injury by regulating key antioxidant proteins, catalase (CAT) and the superoxide dismutases (SOD1 and SOD2). In first trimester placental explants, localization of CAT was limited to cytotrophoblasts, whereas SOD1 was expressed in both the cyto- and syncytiotrophoblasts. In first trimester placental explants, hypoxia decreased the expression of both SOD1 and SOD2, and increased apoptosis. Treatment with rosiglitazone dose-dependently upregulated anti-oxidative CAT and SOD2, and rescued hypoxic injury in first trimester villous explants and JEG-3 cells, strongly suggesting the involvement of the PPARγ in regulating their expressions. Rosiglitazone facilitated transcription activity of PPARγ, and enhanced promotor binding, increased transcriptional activity at the CAT promoter, and elevated protein expression/activity. Treatment of hypoxic JEG-3 cells with rosiglitazone resulted in mitochondrial membrane potential increase and a reduction of caspase 9 and caspase 3 activity which is consistent with improved cell survival. To complement PPARγ activation data, we also utilized the antagonist (SR-202) and siRNA to suppress PPARγ expression and demonstrate the specific role of PPARγ in reducing ROS and oxidative stress. Ex vivo examination of term human placenta revealed lower expression of antioxidant proteins in pathologic compared to healthy placental tissues, which could be rescued by rosiglitazone, indicating that rosiglitazone can improve survival of the trophoblast under pathological conditions. These findings provide evidence that the PPARγ pathway directly influences cellular antioxidants production and the pathophysiology of placental oxidative stress.
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