Gene expression profiling of cutaneous wound healing
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BioMed Central
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Research
Gene expression profiling of cutaneous wound healing Kavita Deonarine1, Monica C Panelli1, Mitchell E Stashower2, Ping Jin1, Kina Smith1, Herbert B Slade3, Christopher Norwood, Ena Wang1, Francesco M Marincola1 and David F Stroncek*1 Address: 1Immunogenetics Section, Department of Transfusion Medicine, Clinical Center National Institutes of Health, Bethesda MD, 20892, USA, 2The Clinical Skin Center of Northern Virginia, Fairfax, VA, 22033, USA and 3DFB Pharmaceuticals, Fort Worth, TX, 76107, USA Email: Kavita Deonarine - [email protected]; Monica C Panelli - [email protected]; Mitchell E Stashower - [email protected]; Ping Jin - [email protected]; Kina Smith - [email protected]; Herbert B Slade - [email protected]; Christopher Norwood - [email protected]; Ena Wang - [email protected]; Francesco M Marincola - [email protected]; David F Stroncek* - [email protected] * Corresponding author
Published: 21 February 2007 Journal of Translational Medicine 2007, 5:11
doi:10.1186/1479-5876-5-11
Received: 16 November 2006 Accepted: 21 February 2007
This article is available from: http://www.translational-medicine.com/content/5/1/11 © 2007 Deonarine et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Although the sequence of events leading to wound repair has been described at the cellular and, to a limited extent, at the protein level this process has yet to be fully elucidated. Genome wide transcriptional analysis tools promise to further define the global picture of this complex progression of events. Study Design: This study was part of a placebo-controlled double-blind clinical trial in which basal cell carcinomas were treated topically with an immunomodifier – toll-like receptor 7 agonist: imiquimod. The fourteen patients with basal cell carcinoma in the placebo arm of the trial received placebo treatment consisting solely of vehicle cream. A skin punch biopsy was obtained immediately before treatment and at the end of the placebo treatment (after 2, 4 or 8 days). 17.5K cDNA microarrays were utilized to profile the biopsy material. Results: Four gene signatures whose expression changed relative to baseline (before wound induction by the pre-treatment biopsy) were identified. The largest group was comprised predominantly of inflammatory genes whose expression was increased throughout the study. Two additional signatures were observed which included preferentially pro-inflammatory genes in the early post-treatment biopsies (2 days after pre-treatment biopsies) and repair and angiogenesis genes in the later (4 to 8 days) biopsies. The fourth and smallest set of genes was down-regulated throughout the study. Early in wound healing the expression of markers of both M1 and M2 ma
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