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Estrogen Receptor-α Mediates the Effects of Estradiol on Telomerase Activity in Human Mesenchymal Stem Cells

Sex steroid hormone receptors play a central role in modulating telomerase activity, especially in cancer cells. However, information on the regulation of steroid hormone receptors and their distinct functions on telomerase activity within the mesenchymal stem cell are largely unavailable due to low...

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Bibliographic Details
Published in:Molecules and cells 2008, 26(5), , pp.454-458
Main Authors: Cha, Y. (Pochon CHA University, Seoul, Republic of Korea), Kwon, S.J. (Pochon CHA University, Seoul, Republic of Korea), Seol, W.G. (Inje University, Busan, Republic of Korea), Park, K.S. (Pochon CHA University, Seoul, Republic of Korea), E-mail: kspark@cha.ac.kr
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Language:English
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Summary:Sex steroid hormone receptors play a central role in modulating telomerase activity, especially in cancer cells. However, information on the regulation of steroid hormone receptors and their distinct functions on telomerase activity within the mesenchymal stem cell are largely unavailable due to low telomerase activity in the cell. In this study, the effects of estrogen (E₂) treatment and function of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) on telomerase activity were investigated in human mesenchymal stem cells (hMSCs). Telomerase activity and mRNA expression of the catalytic subunit of telomerase (hTERT) were upregulated by treatment of the cells with E₂. The protein concentration of ERα was also increased by E₂ treatment, and enhancement of ERα accumulation in the nucleus was clearly detected with immunocytochemistry. When ERα expression was reduced by siRNA transfection into hMSCs, the effect of E₂ on the induction of hTERT expression and telomerase activity was diminished. In contrast, the transient overexpression of ERα increased the effect of E₂ on the expression of hTERT mRNA. These findings indicate that the activation of hTERT expression and telomerase activity by E₂ in hMSCs depends on ERα, but not on ERβ.
ISSN:1016-8478
0219-1032
DOI:10.1016/S1016-8478(23)14021-0