ArticleMolecular endocrinology (Baltimore, Md.)2013
Glucocorticoid receptor signaling contributes to constitutive activation of the noncanonical NF-κB pathway in term human placenta.
Article in Molecular endocrinology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 29 citations in OpenAlex.
- Transcriptomic signatures in tetrapartite brain region identifies shared and unique gene signatures for substance-use.Frontiers in cellular neuroscience · 2026Article
- Characterization of methylation profiles in spontaneous preterm birth placental villous tissue.PloS one · 2023Article
- Expression of nuclear factor kappa B in ovine maternal inguinal lymph nodes during early pregnancy.BMC veterinary research · 2022Article
- Spontaneous preterm birth: Involvement of multiple feto-maternal tissues and organ systems, differing mechanisms, and pathways.Frontiers in endocrinology · 2022Review
- Placental CRH as a Signal of Pregnancy Adversity and Impact on Fetal Neurodevelopment.Frontiers in endocrinology · 2021Review
- Fetal Exosomal Platelet-activating Factor Triggers Functional Progesterone Withdrawal in Human Placenta.Reproductive sciences (Thousand Oaks, Calif.) · 2021Article
- Alterations in endogenous progesterone metabolism associated with spontaneous very preterm delivery.Human reproduction open · 2020Article
- Fetal lung C4BPA induces p100 processing in human placenta.Scientific reports · 2019Article
- Screening a small molecule library to identify inhibitors of NF-κB inducing kinase and pro-labor genes in human placenta.Scientific reports · 2018Article
- Tocolysis: Present and future treatment options.Seminars in perinatology · 2017Review
- Promoter Methylation Pattern Controls Corticotropin Releasing Hormone Gene Activity in Human Trophoblasts.PloS one · 2017Article
- Mono-(2-Ethylhexyl) Phthalate Promotes Pro-Labor Gene Expression in the Human Placenta.PloS one · 2016Article
- Comparative Immunohistochemistry of Placental Corticotropin-Releasing Hormone and the Transcription Factor RelB-NFκB2 Between Humans and Nonhuman Primates.Comparative medicine · 2015Article
- NIK is required for NF-κB-mediated induction of BAG3 upon inhibition of constitutive protein degradation pathways.Cell death & disease · 2015Article
- Reversal of corticosteroid insensitivity by p38 MAPK inhibition in peripheral blood mononuclear cells from COPD.International journal of chronic obstructive pulmonary disease · 2015Article
- Glucocorticoid-induced reversal of interleukin-1β-stimulated inflammatory gene expression in human oviductal cells.PloS one · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our recent study demonstrated that constitutively activated RelB/NF-κB2 positively regulates the CRH in the human placenta. In the current study, we explored the role of the glucocorticoid receptor (GR) signaling in constitutive activation of the noncanonical NF-κB pathway. A glucocorticoid response element (GRE) motif search suggests that both NF-κB inducing kinase (NIK) and RelB genes, which are key regulators of the noncanonical NF-κB pathway, have a putative GRE within their promoter, approximately 1 kb upstream from the transcription start site. By using chromatin immunoprecipitation assay we identified that the GR and phosphorylated GR at Ser211 were associated with the GREs of both NIK and RelB. Dexamethasone stimulated expression of NIK, RelB, NF-κB2 as well as CRH and cyclooxygenase-2 (COX-2). Repression of GR by short interfering RNA resulted in inhibition of NIK, RelB, NF-κB2, CRH, and COX-2. In addition, depletion of GR attenuated glucocorticoid-mediated up-regulation of NIK, RelB, NF-κB2, CRH, and COX-2. Furthermore, siRNA specifically targeting NIK down-regulated CRH and COX-2. Taken together, these results suggest that constitutive activation of the noncanonical NF-κB pathway in term human placenta is driven by the GR signaling, which in turn up-regulates placental CRH and other NF-κB-responsive genes.
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