Chan Jin Park, Ji-Eun Oh, PoChing Lin, Sherry Zhou, Mary Bunnell, Emmanuel Bikorimana, Michael J Spinella, Hyunjung Jade Lim, CheMyong J Ko
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引用次数: 0
Abstract
This study uncovers a dynamic shift in estrogen receptor expression during granulosa cell (GC) differentiation in the ovary, highlighting a transition from estrogen receptor alpha (ESR1) to estrogen receptor beta (ESR2). Using a transgenic mouse model with Esr1-iCre-mediated Esr2 deletion, we demonstrate that ESR2 expression is absent in GCs derived from ESR1-expressing ovarian surface epithelium (OSE) cells. Single-cell analysis of the OSE-GC lineage reveals a developmental trajectory from Esr1-expressing OSE cells to Foxl2-expressing pre-GCs, culminating in GCs exclusively expressing Esr2. Transcriptome analyses identified vasculature-derived TGFβ1 ligands as key regulators of this transition. Supporting this, TGFβ1 treatment of cultured embryonic ovaries reduced Esr1 expression while promoting Esr2 expression. This study underscores the capability of GCs to switch from ESR1 to ESR2 expression as a fundamental aspect of normal differentiation.
期刊介绍：
The mission of Endocrinology is to be the authoritative source of emerging hormone science and to disseminate that new knowledge to scientists, clinicians, and the public in a way that will enable "hormone science to health." Endocrinology welcomes the submission of original research investigating endocrine systems and diseases at all levels of biological organization, incorporating molecular mechanistic studies, such as hormone-receptor interactions, in all areas of endocrinology, as well as cross-disciplinary and integrative studies. The editors of Endocrinology encourage the submission of research in emerging areas not traditionally recognized as endocrinology or metabolism in addition to the following traditionally recognized fields: Adrenal; Bone Health and Osteoporosis; Cardiovascular Endocrinology; Diabetes; Endocrine-Disrupting Chemicals; Endocrine Neoplasia and Cancer; Growth; Neuroendocrinology; Nuclear Receptors and Their Ligands; Obesity; Reproductive Endocrinology; Signaling Pathways; and Thyroid.
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