HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lui, W.-Y. Articles by Cheng, C Y. Search for Related Content PubMed PubMed Citation Articles by Lui, W.-Y. Articles by Cheng, C Y.

¹ Population Council, Center for Biomedical Research, 1230 York Avenue, New York, New York 10021, USA
² Department of Zoology, University of Hong Kong, Hong Kong, China

(Requests for offprints should be addressed to C Yan Cheng; Email: Y-Cheng{at}popcbr.rockefeller.edu)

Wing-Yee Lui’s present address is Department of Zoology, Faculty of Science, University of Hong Kong, Hong Kong, China

Earlier studies have shown that germ cells or germ cell-conditioned media are capable of regulating ₂-macroglobulin (₂-MG, a non-specific protease inhibitor) expression by Sertoli cells and hepatocytes cultured in vitro. These results illustrate a possible physiological link between testes and liver regarding ₂-MG production. Using a series of surgical procedures including castration, hemicastration, and hepatectomy coupled with Northern blot and immunoblot analyses, we report herein that the surge in ₂-MG expression in the liver in response to inflammation is indeed regulated, at least in part, by the testis via testosterone. It was found that hepatectomy induced at least a tenfold increase in the steady-state mRNA and protein production of ₂-MG in the liver. However, castration induced a mild but not statistically significant induction of ₂-MG in the liver in contrast to sham operation or hemicastration alone, when hemicastration alone could induce liver ₂-MG production by almost fourfold. Perhaps most important of all, hepatectomy accompanied by castration significantly reduced the liver ₂-MG response to the surgery-induced inflammation compared with hepatectomy alone, illustrating that the removal of the testicles can induce a loss of signal communications between the testis and the liver, rendering a significant loss of the ₂-MG response to experimentally induced inflammation in the liver. Interestingly, this lack of response of the liver to surgery-induced inflammation regarding ₂-MG production following castration could be restored, at least in part, by using testosterone implants placed subdermally 6 days prior to orchiectomy. Collectively, these results illustrate that a physiological link does indeed exist between the testis and the liver, and that testes per se can influence the liver in vivo ₂-MG expression in response to inflammation possibly via testosterone or testosterone-induced biological factor(s).