Expression data from untreated and rottlerin-treated normal and systemic sclerosis-derived human fibroblasts

PKC-δ inhibition with the selective inhibitor, rottlerin, resulted in potent downregulation of type I collagen expression and production in normal human dermal fibroblasts and abrogated the exaggerated type I collagen production and expression in fibroblasts cultured from affected skin from patients with the fibrosing disorder, systemic sclerosis (SSc). To elucidate the mechanisms involved in the ability of PKC-δ to regulate collagen production in fibroblasts, we examined the effects of PKC-δ inhibition on the transcriptome of normal and SSc-derived human dermal fibroblasts. We used microarrays to detail the effects of PKC-δ inhibition with rottlerin on the transcriptome of normal and SSc-derived human dermal fibroblasts and to identify gene networks that might be involved in the regulation of extracellular matrix by PKC-δ. Early passage normal and SSc human dermal fibroblasts were incubated with rottlerin (50 µg/mL) for 24 hours, followed by RNA extraction of treated and untreated samples and hybridization on Affymetrix microarrays. Early passage fibroblasts derived from normal and SSc dermal biopsies were utilized in this study to ensure that phenotypes remained as close as possible to original biopsy tissue. SSc patient sample biopsies were isolated from leading edge of forearm lesion; normal biopsies were obtained from forearm dermis.