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Submitted on August 11, 2005
Accepted on November 30, 2005
State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China, Division of Endocrinology, Department of Medicine, Harbor-University of California-Los Angeles Medical Center and Los Angeles Biomedical Research Institute, Torrance, California 90509, USA, Graduate School of the Chinese Academy of Sciences, Beijing 100039, China
* To whom correspondence should be addressed. E-mail: liuyx{at}ioz.ac.cn.
Sertoli cell plays a key role in triggering and regulating process of spermatogenesis. Failure of a Sertoli cell to mature functionally will presumably render it incapable of supporting germ cell survival and development that appeared after puberty. Expression of cytokeratin 18 (ck-18) intermediate filaments indicates a state of undifferentiation usually observed in Sertoli cells of prepubertal testis. In this study we have demonstrated that local testicular heat treatment of adult monkey with 43C water for 30 min once daily for 2 consecutive days was capable of activating re-expression of ck-18 in Sertoli cells, that was coincident with activation of ERK1/2 and Akt kinases. Using primary Sertoli cell culture isolated from adult monkey testis, we have further confirmed that the 43 C heat treatment of the cells could also induce ck-18 re-expression, which was similar to the in vivo treatment. ERK MAP kinase was also induced by the heat treatment in a time- and PKA-dependent manner. After blocking ERK MAP kinase signaling pathway, an inhibition of ck-18 expression in the cultured Sertoli cells was observed, and this inhibitory effect was also detected by blocking the PKA activation. However, ck-18 activation in Sertoli cells remained unaltered when PI3K/Akt pathway was blocked. In conclusion, the heat treatment of adult monkey Sertoli cells are capable of inducing a reversible change in the Sertoli cells from an adult differentiated state to an immature-like dedifferentiated state through PKA-ERK MAP kinase-dependent pathways, but not via PI3K/Akt pathway.
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