Estrogen Receptor α Regulates β-Cell Formation During Pancreas Development and Following Injury | Zendy

Yixing Yuchi | Zendy; Ying Cai | Zendy; Bart Legein | Zendy; Sofie De Groef | Zendy; Gunter Leuckx | Zendy; Violette Coppens | Zendy; Eva Van Overmeire | Zendy; Willem Staels | Zendy; Nico De Leu | Zendy; Geert A. Martens | Zendy; Jo A. Van Ginderachter | Zendy; Harry Heimberg | Zendy; Mark Van de Casteele | Zendy

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Estrogen Receptor α Regulates β-Cell Formation During Pancreas Development and Following Injury

Author(s) -

Yixing Yuchi,

Ying Cai,

Bart Legein,

Sofie De Groef,

Gunter Leuckx,

Violette Coppens,

Eva Van Overmeire,

Willem Staels,

Nico De Leu,

Geert A. Martens,

Jo A. Van Ginderachter,

Harry Heimberg,

Mark Van de Casteele

Publication year - 2015

Publication title -

diabetes

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.219

H-Index - 330

eISSN - 1939-327X

pISSN - 0012-1797

DOI - 10.2337/db14-1798

Subject(s) - estrogen receptor , pancreas , microbiology and biotechnology , progenitor cell , enteroendocrine cell , biology , embryonic stem cell , medicine , endocrinology , cell , estrogen , endocrine system , stem cell , gene , hormone , biochemistry , genetics , cancer , breast cancer

Identifying pathways for β-cell generation is essential for cell therapy in diabetes. We investigated the potential of 17β-estradiol (E2) and estrogen receptor (ER) signaling for stimulating β-cell generation during embryonic development and in the severely injured adult pancreas. E2 concentration, ER activity, and number of ERα transcripts were enhanced in the pancreas injured by partial duct ligation (PDL) along with nuclear localization of ERα in β-cells. PDL-induced proliferation of β-cells depended on aromatase activity. The activation of Neurogenin3 (Ngn3) gene expression and β-cell growth in PDL pancreas were impaired when ERα was turned off chemically or genetically (ERα−/−), whereas in situ delivery of E2 promoted β-cell formation. In the embryonic pancreas, β-cell replication, number of Ngn3+ progenitor cells, and expression of key transcription factors of the endocrine lineage were decreased by ERα inactivation. The current study reveals that E2 and ERα signaling can drive β-cell replication and formation in mouse pancreas.

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