Dermal fibroblasts from venous ulcers are unresponsive to the action of transforming growth factor-β 11Supported by grants from the National Institutes of Health (AR42936 and AG10998) and the Dermatology Foundation of Miami.1-Reference-Cited by-同舟云学术

Dermal fibroblasts from venous ulcers are unresponsive to the action of transforming growth factor-β 11Supported by grants from the National Institutes of Health (AR42936 and AG10998) and the Dermatology Foundation of Miami.1

Published:1997-11 Issue:1 Volume:16 Page:59-66
ISSN:0923-1811
Container-title:Journal of Dermatological Science
language:en
Short-container-title:Journal of Dermatological Science

Author:

Hasan Anthony,Murata Hiroshi,Falabella Anna,Ochoa Sofia,Zhou Linda,Badiavas Evangelos,Falanga Vincent

Publisher

Elsevier BV

Subject

Dermatology,Molecular Biology,Biochemistry

Reference23 articles.

1. Falanga V, Eaglstein WH: The trap hypothesis of venous ulceration. Lancet 341: 1006–1008, 1993.

2. Falanga V, Kruskal JB, Franks JJ: Fibrin and fibrinogen-related antigens in patients with venous disease and venous ulceration. Arch Dermatol 127: 75–78, 1991.

3. Browse NL, Burnand KG: The cause of venous ulceration. Lancet 2: 243–245, 1982.

4. Coleridge-Smith PD, Thomas P, Scurr JH, Dormandy JA: Causes of venous ulceration: a new hypothesis? Br Med J 296: 1726–1727, 1988.

5. Grinnell F, Ho C-H, Wysocki A: Degradation of fibronectin and vitronectin in chronic wound fluid: Analysis by cell blotting, immunoblotting, and cell adhesion assays. J Invest Dermatol 98: 410–416, 1992.

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