Skip Navigation



ToxSci Advance Access published online on September 22, 2007

Toxicological Sciences, doi:10.1093/toxsci/kfm246
This Article
Right arrow Advance Access manuscript (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
103/1/4    most recent
kfm246v1
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 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
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Ramaiah, S. K.
Right arrow Articles by Rittling, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ramaiah, S. K.
Right arrow Articles by Rittling, S.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Pathophysiological Role of Osteopontin in Hepatic Inflammation, Toxicity and Cancer

Shashi K. Ramaiah, DVM, PhD, Diplomate ACVP, DABT*,1 and Susan Rittling, PhD2

1 Assistant Professor, Department of Pathobiology, College of Veterinary Medicine, Texas A&M University, MS- 4467, College Station, TX 77843-4467, Tel: (979) 458-4725; Fax: (979) 845-9972 2 Associate Member of the Staff, The Forsyth Institute, Boston MA 02115

* Author for correspondence E-mail: sramaiah{at}cvm.tamu.edu

Received July 6, 2007; revision received September 10, 2007; accepted September 14, 2007


   Abstract

Osteopontin (OPN) is a highly modified integrin-binding extracellular matrix glycophosphoprotein produced by cells of the immune system, epithelial tissue, smooth muscle cells, osteoblasts and tumor cells. Extensive research has elucidated the pivotal role of OPN in cell signaling that controls inflammation, tumor progression and metastasis. OPN interaction with the integrin receptors expressed on inflammatory cells through its RGD and non-RGD motifs promote migration and adhesion of cells. In the liver, it has been reported that hepatic Kupffer cells secrete OPN facilitating macrophage infiltration into necrotic areas following carbon tetrachloride liver toxicity. Recent work has highlighted the role of OPN in inflammatory liver diseases such as alcoholic and non alcoholic liver disease and T-cell mediated hepatitis. The role of OPN in hepatocellular carcinoma has also generated significant interest especially with regards to its role as a prognostic factor. OPN therefore appear to play an important role during liver inflammation and cancer. In this review we will present data to demonstrate the key role played by OPN in mediating hepatic inflammation (neutrophils, monocytes/macrophages and lymphocytes) and its role in hepatocellular carcinoma. Greater understanding of the pathophysiologic role of OPN in hepatic inflammation and cancer may enable development of novel inflammation and cancer treatment strategies.

Key Words: Hepatic injury; hepatic carcinoma; inflammation; neutrophils; osteopontin.


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
Clin. Cancer Res.Home page
D. J. Caruso, A. J.K. Carmack, V. B. Lokeshwar, R. C. Duncan, M. S. Soloway, and B. L. Lokeshwar
Osteopontin and Interleukin-8 Expression is Independently Associated with Prostate Cancer Recurrence
Clin. Cancer Res., July 1, 2008; 14(13): 4111 - 4118.
[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.