The major cause of fibrotic scar is aberrant signalling that can occur during wound healing progression and TGF-beta and FGF-2 are considered as key cytokines. Our lab has recently shown that LTBP-2, an extracellular matrix component, can upregulate TGF-beta expression in skin fibroblasts. LTBP-2 is also upregulated in fibrotic skin lesions where it co-localises (and binds) with FGF-2. In this study we firstly present data comparing gene profiles of LTBP-2, fibrogenic cytokines (TGF-beta, FGF-2), and fibrotic gene markers (smooth muscle action, FBN-1&2, and Col 1&3) in fibroblasts from normal skin and adjacent keloid or hypertrophic scar lesions. Surprisingly the expression patterns of some fibrotic genes markers were similar in normal fibroblasts and fibrotic lesions derived fibroblasts, and SMA and Col 3 had higher expression levels in normal skin fibroblasts. This suggests that the lesion fibroblasts were not retaining their fibrotic phenotypes in culture and that microenviromental factors maybe important to maintain fibrotic characteristics. We then report the effects of LTBP-2 gene knock downs on these cells. FBN-1 and Col1 were elevated in both LTBP-2 knockdown and negative control groups which suggests the upregulation of these two genes was caused by non-specific transcription. TGF-beta and the rest of the target genes expression were not altered in the fibroblasts from both normal and fibrotic origins. Finally, we show that the addition of exogenous LTBP2 upregulated TGF-beta synthesis in the fibroblasts from the fibrotic lesions (as was previously found for normal fibroblasts), indicating that the lesion fibroblasts retained the LTBP-2 receptor responsible for TGF-beta elevation. However, exogenous LTBP-2 did not elevate other fibrotic gene markers. The future approach will aim to establish a cellular model of fibrosis where a fibrotic phenotype can be maintained.