Nephrogenic systemic fibrosis is associated with transforming growth factor β and Smad without evidence of renin-angiotensin system involvement - 24/04/13
, Matthew Petitt, DO, Ramon Sanchez, MD
Reprint requests: Brent Kelly, MD, University of Texas Medical Branch, 301 University Blvd, 4.112 McCollough Bldg, Galveston, TX 77555-0783.Abstract |
Background |
The mechanisms of fibrosis associated with nephrogenic systemic fibrosis (NSF) are largely unknown. Transforming growth factor beta (TGF-β), a known profibrotic cytokine, is theorized to play a central role. The renin-angiotensin system has been linked with both TGF-β expression and fibrosis in other organ systems.
Objective |
We sought to investigate whether these mechanisms were involved with NSF.
Method |
Eleven biopsy specimens from 8 patients with NSF were evaluated by immunohistochemistry for the expression of TGF-β, Smad 2/3, angiotensin-converting enzyme (ACE), and angiotensin II receptor 1 (AT1).
Results |
TGF-β was detected in 8 of 11 samples of NSF. Smad 2/3 nuclear staining was seen in 8 of 11 samples. Conversely, only faint staining for ACE was seen in 2 of the 11 specimens. No AT1 staining was seen.
Limitations |
We did not perform our studies on a cohort of comparable patients with renal dysfunction without NSF. Our technique may not have been sufficiently sensitive to detect renin-angiotensin system involvement.
Conclusions |
TGF-β, as well as its second messengers, Smad 2/3, appears to be associated with the fibrosis seen in NSF. No definitive evidence of renin-angiotensin system involvement could be determined.
Le texte complet de cet article est disponible en PDF.Abbreviations used : ACE, Ang, AT1, Gd, NSF, TGF-β
Plan
| Funding sources: None. |
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| Conflicts of interest: None declared. |
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| This work was presented at the Medical Dermatologic Society meeting held during the 2008 American Academy of Dermatology meeting in San Antonio, Tex. |
Vol 58 - N° 6
P. 1025-1030 - juin 2008 Retour au numéro
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