The Influence of the Anabolic Agent, Oxandrolone, upon the Expression of Procollagen Types I and III mRNA in Human Fibroblasts Cultured on Collagen or Plastic

Journal Article (Journal Article)

The repair process entails the reestablishment of a connective tissue matrix, a scar, where collagen is the major matrix component. Collagen deposition is critical for the initial gains in wound breaking strength and makes up the extracellular matrix of granulation tissue. The systemic administration of anabolic steroid reportedly enhances wound repair through the expansion of collagen synthesis and deposition. Do human dermal fibroblasts receiving an anabolic steroid, oxandrolone, increase their expression of procollagen mRNA? Human dermal fibroblasts were grown on collagencoated or uncoated plastic dishes in the presence of ascorbic acid to optimize collagen processing. By Northern Blot analysis, fibroblasts growing on collagen expressed less types I and III procollagen mRNA, reduced by 49 percent and 91 percent respectively, compared to fibroblasts growing on plastic. Fibroblasts growing on plastic and receiving oxandrolone (3γ/mL) showed a minimal change in procollagen mRNA expression. However, oxandrolone stimulated expression of type III procollagen mRNA 11-fold and type I procollagen mRNA doubled in fibroblasts maintained on collagen, relative to control fibroblasts maintained on collagen. A collagen substrate inhibits types I and III procollagen mRNA expression in fibroblasts. The anabolic steroid, oxandrolone, antagonizes such collagen substrate inhibition of procollagen mRNA expression, stimulating procpllagen mRNA expression to levels of fibroblasts growing on plastic. These findings suggest that oxandrolone may directly enhance wound healing by increasing the expression of procollagen mRNA in fibroblasts associated with a collagen matrix analogous to the healing wound.

Duke Authors

Cited Authors

  • Saggers, GC; Allison, GM; Levinson, H; Kramer, T; Mackay, DR; Ehrlich, HP

Published Date

  • January 1, 2000

Published In

Volume / Issue

  • 13 / 2

Start / End Page

  • 66 - 71

International Standard Serial Number (ISSN)

  • 1044-7946

Citation Source

  • Scopus