ArticleReproduction (Cambridge, England)2020
Core clock gene Bmal1 deprivation impairs steroidogenesis in mice luteinized follicle cells.
Article in Reproduction (Cambridge, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- BMAL1 Dysregulation as a Contributing Mechanism Linking Obesity to Oocyte and Endometrial Dysfunction in IVF.International journal of molecular sciences · 2026Review
- Review
- FTO-mediated NR1D1 mScientific reports · 2026Article
- Sleep traits and risk of premature ovarian insufficiency - two-sample and multivariate mendelian randomisation analysis.Przeglad menopauzalny = Menopause review · 2025Article
- The interplay between the PI3K/AKT pathway and circadian clock in physiologic and cancer-related pathologic conditions.Cell proliferation · 2024Review
- Period circadian regulator 2-mediated steroid hormone synthesis by regulating transcription of steroidogenic acute regulatory protein in porcine granulosa cells.Journal of animal science · 2024Article
- Role of Melatonin in Bovine Reproductive Biotechnology.Molecules (Basel, Switzerland) · 2023Review
- Continuous artificial light potentially disrupts central and peripheral reproductive clocks leading to altered uterine physiology and reduced pregnancy success in albino mice.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2022Article
- Impact of sleep patterns upon female neuroendocrinology and reproductive outcomes: a comprehensive review.Reproductive biology and endocrinology : RB&E · 2022Review
- Acute hypoxia induced dysregulation of clock-controlled ovary functions.Frontiers in physiology · 2022Article
- Critical Roles of the Circadian Transcription FactorFrontiers in endocrinology · 2022Review
- Circadian Rhythms Within the Female HPG Axis: From Physiology to Etiology.Endocrinology · 2021Review
- Comparison of expression patterns of six canonical clock genes of follicular phase and luteal phase in Small-tailed Han sheep.Archives animal breeding · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Luteinization is the event of corpus luteum formation, a way of follicle cells transformation and a process of steroidogenesis alteration. As the core clock gene, Bmal1 was involved in the regulation of ovulation process and luteal function afterwards. Till now, the underlying roles of luteinization played by Bmal1 remain unknown. To explore the unique role of Bmal1 in luteal steroidogenesis and its underlying pathway, we investigated the luteal hormone synthesis profile in Bmal1 knockout female mice. We found that luteal hormone synthesis was notably impaired, and phosphorylation of PI3K/NfκB pathway was significantly activated. Then, the results were verified in in vitro cultured cells, including isolated Bmal1 interference granulosa cells (GCs) and theca cells (TCs), respectively. Hormones levels of supernatant culture media and mRNA expressions of steroidogenesis-associated genes (star, Hsd3β2, cyp19a1 in GCs, Lhcgr, star, Hsd3β2, cyp17a1 in TCs) were mutually decreased, while the phosphorylation of PI3K/NfκB was promoted during in vitro luteinization. After PI3K specific-inhibitor LY294002 intervention, mRNA expressions of Lhcgr and Hsd3β2 were partially rescued in Bmal1 interference TCs, together with significantly increased androstenedione and T synthesis. Further exploration in TCs demonstrated BMAL1 interacted directly but negatively with NfκB p65 (RelA), a subunit which was supposed as a mediator in Bmal1-governed PI3K signaling regulation. Taken together, we verified the novel role of Bmal1 in luteal steroidogenesis, achieving by negative interplay with RelA-mediated PI3K/NfκB pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.