spacer gif spacer gif spacer gif spacer gif Propose a workshop for 2011 spacer gif
QUICK SEARCH:   [advanced]


spacer gif
     Home     Help     Feedback     Subscriptions     Archive     Search    

The fully linked HTML version of this article has now been published.
JCS ePress online publication date 3 Feb 2004
doi: 10.1242/jcs.00932

This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jcs.00932v1
117/6/849    most recent
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 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 Santiago-Josefat, B.
Right arrow Articles by Fernandez-Salguero, P. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Santiago-Josefat, B.
Right arrow Articles by Fernandez-Salguero, P. M.
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   Add to Twitter  
What's this?

Research Article

Overexpression of latent transforming growth factor-{beta} binding protein 1 (LTBP-1) in dioxin receptor-null mouse embryo fibroblasts


Belen Santiago-Josefat, Sonia Mulero-Navarro, Sarah L. Dallas, and Pedro M. Fernandez-Salguero*
* Author for correspondence (e-mail: pmfersal{at}unex.es)

The aryl hydrocarbon receptor (AhR) is a transcriptional regulator of genes involved in xenobiotic metabolism. Increasingly clear is also the role of the AhR in the control of cell growth and proliferation. By analyzing differential patterns of gene expression between wild-type (AhR+/+) and null (AhR-/-) mouse embryo fibroblasts (MEF), we have identified latent transforming growth factor-{beta} binding protein 1 (LTBP-1) as a negatively AhR-regulated gene in the absence of xenobiotics. Ltbp-1 mRNA and protein expression were markedly increased in AhR-/- MEF. Furthermore, secreted LTBP-1 was elevated in the culture medium and the extracellular matrix of AhR-null MEF. Actinomycin D inhibited Ltbp-1 mRNA overexpression, suggesting regulation at the transcriptional level. AhR activation by dioxin (TCDD) downregulated Ltbp-1, again suggesting an AhR-regulated mechanism. Treatment of AhR+/+ MEF with transforming growth factor-{beta} (TGF-{beta}) downregulated AhR and, simultaneously, increased Ltbp-1, further supporting the role of this receptor in LTBP-1 expression. AhR-/- conditioned medium had higher levels of active and total TGF-{beta} activity, suggesting a role for LTBP-1 in maintaining extracellular TGF-{beta} concentrations. TGF-{beta} did not appear to directly regulate Ltbp-1 given that addition of TGF{beta} neutralizing antibody or TGF{beta} protein to AhR-/- MEF had no effect on Ltbp-1 expression. AhR-/- MEF had lower levels of matrix metalloproteinase 2 (MMP-2) activity, which could not be attributable to MMP-2 mRNA downregulation or MMP-inhibitors Timp-1 and Timp-2 overexpression. These data identify LTBP-1 as one of the few AhR-regulated genes not involved in xenobiotic metabolism and also support the implication of the AhR in controlling TGF{beta} activity and cell proliferation.
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   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
A. C. Roman, J. M. Carvajal-Gonzalez, E. M. Rico-Leo, and P. M. Fernandez-Salguero
Dioxin Receptor Deficiency Impairs Angiogenesis by a Mechanism Involving VEGF-A Depletion in the Endothelium and Transforming Growth Factor-{beta} Overexpression in the Stroma
J. Biol. Chem., September 11, 2009; 284(37): 25135 - 25148.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
J. M. Carvajal-Gonzalez, A. C. Roman, M. I. Cerezo-Guisado, E. M. Rico-Leo, G. Martin-Partido, and P. M. Fernandez-Salguero
Loss of dioxin-receptor expression accelerates wound healing in vivo by a mechanism involving TGF{beta}
J. Cell Sci., June 1, 2009; 122(11): 1823 - 1833.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Biol. CellHome page
J. M. Carvajal-Gonzalez, S. Mulero-Navarro, A. C. Roman, V. Sauzeau, J. M. Merino, X. R. Bustelo, and P. M. Fernandez-Salguero
The Dioxin Receptor Regulates the Constitutive Expression of the Vav3 Proto-Oncogene and Modulates Cell Shape and Adhesion
Mol. Biol. Cell, March 15, 2009; 20(6): 1715 - 1727.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
X. Chang, Y. Fan, S. Karyala, S. Schwemberger, C. R. Tomlinson, M. A. Sartor, and A. Puga
Ligand-Independent Regulation of Transforming Growth Factor {beta}1 Expression and Cell Cycle Progression by the Aryl Hydrocarbon Receptor
Mol. Cell. Biol., September 1, 2007; 27(17): 6127 - 6139.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
B. J. McMillan and C. A. Bradfield
The Aryl Hydrocarbon Receptor sans Xenobiotics: Endogenous Function in Genetic Model Systems
Mol. Pharmacol., September 1, 2007; 72(3): 487 - 498.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Mulero-Navarro, E. Pozo-Guisado, P. A. Perez-Mancera, A. Alvarez-Barrientos, I. Catalina-Fernandez, E. Hernandez-Nieto, J. Saenz-Santamaria, N. Martinez, J. M. Rojas, I. Sanchez-Garcia, et al.
Immortalized Mouse Mammary Fibroblasts Lacking Dioxin Receptor Have Impaired Tumorigenicity in a Subcutaneous Mouse Xenograft Model
J. Biol. Chem., August 5, 2005; 280(31): 28731 - 28741.
[Abstract] [Full Text] [PDF]


© The Company of Biologists Ltd 2004