Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Bell, S.C.
Right arrow Articles by Malak, T.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bell, S.C.
Right arrow Articles by Malak, T.M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Molecular Human Reproduction, Vol. 5, No. 11, 1066-1076, November 1999
© 1999 European Society of Human Reproduction and Embryology

Molecular aspects of pregnancy

Alternatively spliced tenascin-C mRNA isoforms in human fetal membranes

S.C. Bell1,4, J.H. Pringle2, D.J. Taylor1 and T.M. Malak1,3

Preterm Birth Research Group, 1 Department of Obstetrics and Gynaecology, and 2 Department of Pathology, Faculty of Medicine and Biological Sciences, University of Leicester, Leicester LE3 7LX, UK

Abstract

Tenascin-C is an extracellular matrix glycoprotein whose monomers include eight consecutive fibronectin type III-like repeats, encoded by exons 10–16, and which are subject to alternative splicing. Transcripts containing these exons are expressed during tissue wounding and active tissue remodelling. Human fetal membranes have been proposed to undergo active tissue remodelling as part of the mechanisms leading to their rupture and immunoreactive tenascin-C has been detected in this tissue. Employing reverse transcription–polymerase chain reaction (RT–PCR) and exon-specific primers, products corresponding to multiple splicing events in the alternatively spliced region have now been identified. The overall splicing pattern would indicate that the major transcripts correspond to complete exclusion of the alternatively spliced region; inclusion of only exon 16; and inclusion of exons 10–14 and 16, including or excluding exon 12. The sole site in tenascin-C susceptible to cleavage by matrix metalloproteinases (MMP)-2 and MMP-3 is found within the exon 12 encoded repeat, therefore translation of isoforms which include or exclude exon 12 may produce `large' tenascins mediating functions ascribed to this form but susceptible or resistant to these MMPs. The demonstration of expression of `large' tenascin mRNA isoforms supports the concept that fetal membranes at term are a site of active tissue remodelling.

amniochorion/fetal membranes/mRNA/splicing/tenascin-C

Notes

3 Current address Eastbourne General Hospital, Eastbourne, East Sussex, BN21 2UD, UK

4 To whom correspondence should be addressed


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
 Cancer Res.Home page
M. Adams, J. L. Jones, R. A. Walker, J. H. Pringle, and S. C. Bell
Changes in Tenascin-C Isoform Expression in Invasive and Preinvasive Breast Disease
Cancer Res., June 1, 2002; 62(11): 3289 - 3297.
[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.