|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Oestrogen regulates proliferation and differentiation of human islet-derived precursor cells through oestrogen receptor alpha
Zhenhua Ren*†‡, Chunlin Zou*†, Huijun Ji*† and Y Alex Zhang*†1
*Cell Therapy Center, Xuanwu Hospital, Capital Medical University, Beijing, Peoples Republic of China, †Key Laboratory of Neurodegeneration, Ministry of Education, Beijing, Peoples Republic of China, and ‡Department of Anatomy, Anhui Medical University, Hefei 230032, Peoples Republic of China
E2 (oestradiol-17β) is an important hormone that regulates various cell functions including insulin production. hIPCs (human islet-derived precursor cells) are capable of proliferating and differentiating into cells that secrete insulin in response to glucose in vivo and in vitro. However, the effect of E2 on hIPCs is currently unclear. In this study, we found that ERα (oestrogen receptor alpha), but not ERβ, was expressed on hIPCs, and E2 promoted the proliferation and inhibited the differentiation of adult hIPCs. Although fetal hIPCs also express ERα, no effect of E2 on the fetal hIPCs was observed, suggesting differing roles of E2 at different stages of pancreatic development. This study indicates that E2 may be one of the key factors that control the turnover of adult pancreatic β cells by regulating the proliferation and differentiation of adult hIPCs through ERα.
Key words: cell proliferation, cell differentiation, diabetes, human islet-derived precursor cell, oestradiol-17β
Abbreviations: bFGF, basic fibroblast growth factor, BrdU, bromodeoxyuridine, CCK-8, Cell Counting Kit-8, DMEM, Dulbecco’s modified Eagle’s medium, E2, oestradiol-17β, EGF, epidermal growth factor, ER, oestrogen receptor, hIPC, human islet-derived precursor cell, ICC, islet-like cell cluster, KRB, Krebs–Ringer bicarbonate solution, PPT, 4,4',4"-(4-propyl-[1H]-pyrazole-1,3,5-triyl) tris-phenol, RT-PCR, reverse transcription-PCR
1To whom correspondence should be addressed (email email@example.com).
Received 4 November 2009/26 January 2010; accepted 4 February 2010
Published as Cell Biology International Immediate Publication 4 February 2010, doi:10.1042/CBI20090390
© The Author(s) Journal compilation © 2010 Portland Press Limited