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Current Molecular Medicine

Editor-in-Chief

ISSN (Print): 1566-5240
ISSN (Online): 1875-5666

Implication of Differential Peroxiredoxin 4 Expression with Age in Ovaries of Mouse and Human for Ovarian Aging

Author(s): Y. Qian, L. Shao, C. Yuan, C.-Y. Jiang, J. Liu, C. Gao, L. Gao, Y.-G. Cui, S.-W. Jiang, J.-Y. Liu and Y. Meng

Volume 16, Issue 3, 2016

Page: [243 - 251] Pages: 9

DOI: 10.2174/1566524016666160225151647

Price: $65

Abstract

Ovarian aging has been associated with increased levels of reactive oxygen species and the deficiencies of antioxidant defense. The antioxidant peroxiredoxin 4 (Prdx4), as a member of Prdx protein family, controls cellular oxidative stress by reducing H2O2 levels. In previous studies, we provided evidence that Prdx4 was abundantly expressed in mouse and human ovaries and expression of Prdx4 in matured follicles was higher than that in immatured follicles. Accordingly, we speculated that Prdx4 expression could be associated with follicle development and it may be as a part of the antioxidative mechanism in follicular development. In this study, we demonstrated that Prdx4 was mainly expressed in the granulosa cells of mouse ovaries and the expression levels significantly increased along development of follicles. However, the expression levels of Prdx4 decreased when mice reached the aged stage (18 months old). Likewise a similar pattern that was observed in the mice study was also found in human ovaries where Prdx4 was expressed lower in premenopausal women than young women. Subsequent in vitro experiments indicated that Prdx4 mRNA and protein levels both increased with H2O2 in a concentrationdependent manner, but decreased rapidly with high concentration of H2O2, and the changes were closely related to cell proliferation. Taken together, these findings argue our understanding on the role of oxidative stress and antioxidant in follicular development and ovarian aging.

Keywords: Antioxidant, follicular development, granulosa cell, ovarian aging, oxidative stress, peroxiredoxin 4.


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