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Selective reduction of fibrotic markers in repairing corneas of mice deficient in Smad3 by Brian M. Stramer; Jeffrey S. Austin; Anita B. Roberts; M. Elizabeth Fini is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Selective reduction of fibrotic markers in repairing corneas of mice deficient in Smad3 about?

## Abstract The cytokine transforming growth factor‐β (TGF‐β) is a key mediator of fibrosis in all organs. Expression of fibrotic markers in repairing cutaneous wounds is reduced in mice lacking Smad3, a downstream cytoplasmic mediator of TGF‐β signaling (Ashcroft et al., 1999, Nat Cell Biol 1(5):260–266). This is correlated with a reduction in inflammation, and thus in the blood elements thought to be a significant source of TGF‐β at the wound site, the principle form being TGF‐β1. Since the major cellular source of TGF‐β in corneal wounds is the epithelium, and the principal isoform is TGF‐β2, we investigated whether Smad3 deficiency has similar anti‐fibrotic effects on corneal repair. In contrast to the situation of cutaneous repair, expression of the fibrotic marker, fibronectin, was equivalent in corneal repair tissue of Smad3−/− mice as compared to their +/− littermates, even though expression of a second fibrotic marker not previously examined in cutaneous wounds, α‐smooth muscle (sm) actin, was reduced. Also unlike in cutaneous wounds, the inflammatory response was unaffected. These differences between corneal and cutaneous repair correlated with the lack of apparent change

Who reads Selective reduction of fibrotic markers in repairing corneas of mice deficient in Smad3?

Author

Brian M. Stramer; Jeffrey S. Austin; Anita B. Roberts; M. Elizabeth Fini

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0021-9541)

Published

2004

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)