ECEESPE2025 Poster Presentations Pituitary, Neuroendocrinology and Puberty (162 abstracts)
It is quite stressful to be a stem cell
Olivia Sherwin 1,2 , Ilona Berger 1,2 , Emily Scott-Solomon 3 , Bence Kover 1 , Ya-Chieh Hsu 3 , Frederique Ruf-Zamojski 4 , Shinsuke Onuma 4 , Michel Zamojski 4 , Stefan Bornstein 2 , Charlotte Steenblock 2 , Marily Theodoropoulou 5 , Yasmine Kemkem 1 , James Kaufman-Cook 1 , Miriam Vazquez Segoviano 1 & Cynthia Andoniadou 1
1King’s College London, London, United Kingdom; 2Technical University of Dresden, Dresden, Germany; 3Harvard University, Cambridge, United States; 4Cedars-Sinai Medical Center, Los Angeles, United States; 5Ludwig Maximilian University of Munich, Munich, Germany
JOINT2345
The stress response is an adaptive mechanism that results in the release of glucocorticoids from the adrenal cortex, in order to regulate metabolic, immune and inflammatory related processes of the body. The intensity and duration of this response is tightly regulated by the Hypothalamic Pituitary Adrenal (HPA) axis and a pivotal component of this axis is the negative feedback of glucocorticoids. Central to this process, the pituitary gland modulates glucocorticoid levels by adjusting adrenocorticotropic hormone (ACTH) secretion in response to corticotrophin releasing hormone (CRH) from the hypothalamus and glucocorticoid feedback from the bloodstream. Our studies are centred around the response of HPA axis stem cells in mouse under physiological and stress conditions. We present here that SOX2+ anterior pituitary stem cells (PSCs) are responsive to glucocorticoids, activate glucocorticoid receptor (GR) signalling and are implicated in the stress response. To determine the role of GR signalling in PSCs, we generated Sox2CreER/+;GRfl/fl mice, where the GR receptor can be deleted specifically in the stem cells upon administration of a drug, tamoxifen. Combining in vivo and in vitro analyses, we show that PSCs activate GR during an acute stress model, leading to upregulated expression and secretion of cytokines, able to influence neighbouring cells. in vitro data using mouse corticotroph tumour AtT-20 cells and in vivo data from the mouse model, support that GR-dependent signalling regulates the Pomc promoter, in a dose-dependent manner. Together, these data indicate a functional role for GR signalling in SOX2+ pituitary stem cells implicating these cells in paracrine signalling during the stress response.
Volume 110
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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