Journal of Histochemistry and Cytochemistry Priciples for Free Access to Science
  Search:   
    >> Advanced Search

Guidelines | Subscriptions | About | exPRESS - Current - Archive | Business Information | Contact
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
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 Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Whiting, C. V.
Right arrow Articles by Bland, P. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Whiting, C. V.
Right arrow Articles by Bland, P. W.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
Journal of Histochemistry and Cytochemistry, Vol. 51, 1177-1189, September 2003, Copyright © 2003, The Histochemical Society, Inc.


ARTICLE

Abnormal Mucosal Extracellular Matrix Deposition Is Associated with Increased TGF-ß Receptor-expressing Mesenchymal Cells in a Mouse Model of Colitis

Christine V. Whitinga, John F. Tarltona, Michael Baileya, Clare L. Morgana, and Paul W. Blanda,b
a Division of Veterinary Pathology, Infection and Immunity, Department of Clinical Veterinary Science, University of Bristol, Bristol, United Kingdom
b Department of Clinical Immunology, University of Gothenburg, Gothenburg, Sweden

Correspondence to: Christine V. Whiting, Div. of Veterinary Pathology, Infection and Immunity, Dept. of Clinical Veterinary Science, University of Bristol, Bristol BS40 5DU, UK. E-mail: c.v.whiting@bris.ac.uk

Transforming growth factor-ß (TGF-ß) depresses mucosal inflammation and upregulates extracellular matrix (ECM) deposition. We analyzed TGF-ß receptors RI and RII as well as ECM components using the CD4+ T-cell-transplanted SCID mouse model of colitis. The principal change in colitis was an increased proportion of TGF-ß RII+ mucosal mesenchymal cells, predominantly {alpha}-smooth muscle actin (SMA)+ myofibroblasts, co-expressing vimentin and basement membrane proteins, but not type I collagen. TGF-ß RII+ SMA- fibroblasts producing type I collagen were also increased, particularly in areas of infiltration and in ulcers. Type IV collagen and laminin were distributed throughout the gut lamina propria in disease but were restricted to the basement membrane in controls. In areas of severe epithelial damage, type IV collagen was lost and increased type I collagen was observed. To examine ECM production by these cells, mucosal mesenchymal cells were isolated. Cultured cells exhibited a similar phenotype and matrix profile to those of in vivo cells. The data suggested that there were at least two populations of mesenchymal cells responsible for ECM synthesis in the mucosa and that ligation of TGF-ß receptors on these cells resulted in the disordered and increased ECM production observed in colitic mucosa.

(J Histochem Cytochem 51:1177–1189, 2003)

Key Words: extracellular matrix, TGF-ß colitis, mouse model, TGF-ß receptors, intestine, wound healing


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
IOVSHome page
D. W. Esson, M. P. Popp, L. Liu, G. S. Schultz, and M. B. Sherwood
Microarray Analysis of the Failure of Filtering Blebs in a Rat Model of Glaucoma Filtering Surgery
Invest. Ophthalmol. Vis. Sci., December 1, 2004; 45(12): 4450 - 4462.
[Abstract] [Full Text] [PDF]




Guidelines | Subscriptions | About | exPRESS - Current - Archive | Business Information | Contact
The Journal of Histochemistry & Cytochemistry is owned, published, and licensed by The Histochemical Society © 2003