Skip Navigation



Hum. Reprod. Advance Access published online on September 9, 2008
Human Reproduction, doi:10.1093/humrep/den334
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF ) Freely available
Right arrow All Versions of this Article:
24/1/20    most recent
den334v1
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 Liu, D.Y.
Right arrow Articles by Baker, H.W.G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, D.Y.
Right arrow Articles by Baker, H.W.G.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. 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

Enhancement of sperm–zona pellucida (ZP) binding capacity by activation of protein kinase A and C pathways in certain infertile men with defective sperm–ZP binding

D.Y. Liu1,4, M.L. Liu1,2,3 and H.W.G. Baker1,2,3

1 Department of Obstetrics and Gynaecology, University of Melbourne, Australia 2 Reproductive Services, Royal Women's Hospital, Australia 3 Melbourne IVF, Melbourne, Australia

4 Correspondence address. Tel: +61-3-9344-2042; Fax: +61-3-9347-1761; E-mail: dyl{at}unimelb.edu.au

BACKGROUND: Defective sperm–zona pellucida (ZP) binding (DSZPB) is a common cause of failure of fertilization in vitro. This study was to determine if DSZPB is caused by defective pathways upstream of protein kinase A (PKA) and C (PKC), or reduced protein tyrosine phosphorylation (TP).

METHODS: Infertile men with DSZPB and either normal sperm morphology (NSM) ≥ 14% (n = 15) or ≤5% (n = 15) were studied. Sperm–ZP binding test was performed by incubation of motile sperm with oocytes for 2 h with or without dibutyryl cyclic AMP (dbcAMP, PKA activator) or phorbol myristate acetate (PMA, PKC activator). TP of capacitated sperm in medium was assessed by immunofluorescence with an anti-phosphotyrosine monoclonal antibody.

RESULTS: For normal sperm with normal sperm–ZP binding, both PMA and dbcAMP significantly enhanced sperm–ZP binding in a dose–response manner. Only dbcAMP, but not PMA, significantly increased TP of capacitated sperm. In DSZPB men with severe teratozoospermia (NSM ≤ 5%), neither PMA nor dbcAMP enhanced sperm–ZP binding, despite dbcAMP significantly increasing the TP of capacitated sperm for all samples. In contrast, for DSZPB with NSM ≥ 14%, PMA caused significantly increased sperm binding up to normal levels (≥40 sperm bound/ZP) in five men, and dbcAMP had a similar result in two men. Again TP was significantly enhanced only by dbcAMP, but not by PMA.

CONCLUSIONS: There is defective signalling in pathways upstream of PKC and PKA in some men with DSZPB and normal semen analysis. Stimulation of TP by dbcAMP does not enhance sperm–ZP binding capacity in DSZPB men with low TP, regardless of sperm morphology.

Key words: PKC/PKA/tyrosine phosphorylation/sperm–zona binding/male infertility

Submitted on May 12, 2008; resubmitted on August 8, 2008; accepted on August 12, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




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.