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Mitogen-Activated Protein Kinase p38 Pathway in Venous Ulcer Fibroblasts

^* To whom correspondence should be addressed. E-mail: joseph.raffetto{at}med.va.gov.

	Abstract

Objective: Venous ulcer fibroblasts (w-fb) have attenuated growth compared to normal fibroblasts (n-fb). The MAPKp38 pathway mediates stress-responses in various diseases. We hypothesize that p38 pathway is altered in w-fb. Methods: W-fb were isolated from venous ulcers and n-fb from the ipsilateral thigh. Fibroblasts were analyzed for phosphorylated p38 using immunoblot. The relation between p38 and w-fb proliferation was assessed with SB203580 (p38 inhibitor). Fibroblasts were treated with bFGF, TNF-a, and IL-1 and p38 expression analyzed. Results: Phosphorylated p38 expression was increased in w-fb (AU% = 233.5±59.7, P = 0.039) compared to n-fb (AU% = 99.9±14.6). W-fb treated with SB203580 demonstrated increased growth compared to untreated w-fb. W-fb treated with bFGF demonstrated decreased p38. TNF- and IL-1 significantly increase p38 expression. Conclusions: MAPK p38 is up-regulated in w-fb. Regulation of w-fb proliferation is influenced by p38. Altering the p38 pathway in vivo with growth factors or cytokine inhibition may improve fibroblast proliferation and venous ulcer healing.

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