ArticleThe Journal of clinical endocrinology and metabolism2016
Nrf2 Activation Inhibits Effects of Thrombin in Human Amnion Cells and Thrombin-Induced Preterm Birth in Mice.
Article in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- LAMB1 regulates COL3A1 and RAC1 expression during subchorionic hemorrhage progression.BMC biology · 2026Article
- Quantification of the size of subchorionic hematoma causing pregnancy-related complications: a retrospective cohort study.Journal of medical ultrasonics (2001) · 2024Article
- Role of Transcription Factors in the Management of Preterm Birth: Impact on Future Treatment Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Stretch Causes Cell Stress and the Downregulation of Nrf2 in Primary Amnion Cells.Biomolecules · 2022Article
- Novel Insights into the Regulatory Role of Nuclear Factor (Erythroid-Derived 2)-Like 2 in Oxidative Stress and Inflammation of Human Fetal Membranes.International journal of molecular sciences · 2020Article
- Progestins Inhibit Interleukin-1β-Induced Matrix Metalloproteinase 1 and Interleukin 8 Expression via the Glucocorticoid Receptor in Primary Human Amnion Mesenchymal Cells.Frontiers in physiology · 2020Article
- Thrombin Alters Human Endometrial Stromal Cell Differentiation During Decidualization.Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- Mouse models of preterm birth: suggested assessment and reporting guidelines.Biology of reproduction · 2018Review
- Rosiglitazone Regulates TLR4 and Rescues HO-1 and NRF2 Expression in Myometrial and Decidual Macrophages in Inflammation-Induced Preterm Birth.Reproductive sciences (Thousand Oaks, Calif.) · 2017Article
- Nrf2 regulates gene-environment interactions in an animal model of intrauterine inflammation: Implications for preterm birth and prematurity.Scientific reports · 2017Article
- Is Vitamin C Beneficial to Patients with CAP?Current infectious disease reports · 2016Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
contextNrf2 is a key transcription factor that modulates cell defense mechanisms against endogenous and exogenous stress. Previously, we reported that thrombin increased matrix metalloproteinases and prostaglandin synthesis in human amnion mesenchymal cells.
objectiveWe sought to determine whether activation of Nrf2 alters the effect of thrombin on prostaglandin synthesis, protease activation, and cytokine release in human amnion. Furthermore, we analyzed the effect of Nrf2 activation on thrombin-induced preterm labor in mice.
designPrimary human amnion mesenchymal cells and pregnant mice were employed to investigate the effect of Nrf2 on thrombin-induced inflammation and preterm birth.
settingThis was a laboratory-based study using cells and mice.
resultsAs expected, thrombin increased cyclooxygenase-2, IL-1β, IL-6, IL-8, and matrix metalloproteinase-1 in amnion mesenchymal cells. Preincubation with Nrf2 activators, diethyl maleate or 15-deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2), profoundly repressed thrombin-induced gene expression. In addition, Nrf2 activation inhibited thrombin-induced cyclooxygenase-2 protein levels and secretion of prostaglandin E2, IL-1β, IL-6, IL-8, TNFα, and granulocyte-macrophage colony-stimulating factor in the media. Whereas vehicle and 15d-PGJ2 did not alter gestational length, all pregnant mice treated with thrombin delivered preterm. 15d-PGJ2 delayed thrombin-induced preterm birth significantly.
conclusionsThe results indicate that Nrf2 activation represents a key stress response in amnion mesenchyme cells and in pregnant mice to mitigate the adverse proinflammatory effects of thrombin on the fetal membranes. We suggest, therefore, that pharmacological activation of Nrf2 may prevent the increased risk of preterm premature rupture of the membranes associated with thrombin activation that accompanies subchorionic hemorrhage or bleeding during pregnancy.
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