Skip Navigation



Hum. Reprod. Advance Access published online on April 3, 2006
Human Reproduction, doi:10.1093/humrep/del066
This Article
Right arrow FREE Full Text (PDF ) Freely available
Right arrow All Versions of this Article:
21/7/1734    most recent
del066v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Theas, M.S.
Right arrow Articles by Lustig, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Theas, M.S.
Right arrow Articles by Lustig, L.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received December 28, 2005
Revised February 6, 2006
Accepted February 10, 2006

Article

Death receptor and mitochondrial pathways are involved in germ cell apoptosis in an experimental model of autoimmune orchitis

M.S. Theas 1 *, C. Rival 1, S. Jarazo Dietrich 1, V.A. Guazzone 1, and L. Lustig 1

1 Centro de Investigaciones en Reproducción, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina

* To whom correspondence should be addressed.
M.S. Theas, E-mail: ciruba{at}fmed.uba.ar


  Abstract

BACKGROUND: Studies on experimental autoimmune orchitis (EAO) have helped to elucidate immunological mechanisms involved in testicular damage. We previously demonstrated that EAO is characterized by lymphomono-nuclear cell infiltrates and apoptosis of spermatocytes and spermatids expressing Fas and TNFR1. The aim of this work was to characterize the pathways involved in germ cell apoptosis in EAO and to determine the involvement of the Bcl-2 protein family in this process. METHODS AND RESULTS: EAO was induced in rats by immunization with testicular homogenate (TH) and adjuvants, whereas control (C) rats were injected with saline solution and adjuvants. Testis of EAO rats showed procaspase 8 cleavage products (western blot) with high caspase 8 activity. Cyto-chrome c content increased in the cytosol and decreased in the mitochondrial fraction of testis from EAO rats compared with C, concomitant with increased caspase 9 activity. Bax was mainly expressed in spermatocytes and spermatids and Bcl-2 in basal germ cells (immunohistochemistry). Bax{beta} isoform content increased in EAO rat testis compared with C, whereas content of Bax{alpha} remained unchanged (western blot). However, Bax{alpha} content decreased in the cytosol and increased in the mitochondrial and endoplasmic reticulum (ER)-enriched fractions of testis from EAO rats compared with C (western blot). Bcl-2 content also increased in the testes of EAO rats. CONCLUSIONS: Our results demonstrated that extrinsic, mitochondrial and possibly ER pathways are inducers of germ cell apoptosis in EAO and that Bax and Bcl-2 proteins modulate this process.

Keywords: apoptotic pathways/autoimmune orchitis/Bax/Bcl-2/germ cell apoptosis.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Hum ReprodHome page
M.S. Theas, C. Rival, S. Jarazo-Dietrich, P. Jacobo, V.A. Guazzone, and L. Lustig
Tumour necrosis factor-{alpha} released by testicular macrophages induces apoptosis of germ cells in autoimmune orchitis
Hum. Reprod., August 1, 2008; 23(8): 1865 - 1872.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.