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Localisation of oestrogen receptors in stem cells and in stem cell derived neurons of the mouse

Davis, D., Vajaria, R., Delivopoulos, E. ORCID: https://orcid.org/0000-0001-6156-1133 and Vasudevan, N. ORCID: https://orcid.org/0000-0003-4326-3938 (2022) Localisation of oestrogen receptors in stem cells and in stem cell derived neurons of the mouse. Journal of Neuroendocrinology. e13220. ISSN 0953-8194

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To link to this item DOI: 10.1111/jne.13220

Abstract/Summary

Oestrogen receptors (ER) transduce the effects of the endogenous ligand, 17b-estradiol in cells to regulate a number of important processes such as reproduction, neuroprotection, learning and memory and anxiety. The ERa or ERb are classical intracellular nuclear hormone receptors while some of their variants or novel proteins such as the GPCR, GPER1/GPR30 are reported to localise in intracellular as well as plasma membrane locations. Though the brain is an important target for oestrogen with oestrogen receptors expressed differentially in various nuclei, subcellular organisation and crossttalk between these receptors is underexplored. Using an adapted protocol that is rapid, we first generated neurons from mouse embryonic stem cells. Our immunocytochemistry approach shows that the full length ERa (ERa-66) and for the first time, that an ERa variant, ERa-36, as well as GPER1 is present in embryonic stem cells. In addition, these receptors typically decrease their nuclear localisation as neuronal maturation proceeds. Finally, though these ERs are present in many subcellular compartments such as the nucleus and plasma membrane, we show that they are specifically not colocalised with each other, suggesting that they initiate distinct signalling pathways.

Item Type:Article
Refereed:Yes
Divisions:Interdisciplinary Research Centres (IDRCs) > Centre for Integrative Neuroscience and Neurodynamics (CINN)
Life Sciences > School of Biological Sciences > Biomedical Sciences
Life Sciences > School of Biological Sciences > Department of Bio-Engineering
ID Code:109094
Publisher:Wiley

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