Gene Expression Markers of Wound Healing and Oxidative Stress in Keloid
ALFREDO GRAGNANI, MD, PhD, Jessica Bonucci, master student, Marina Nishimuni, medical graduation student, Gibrán E. H. Muñoz, medical graduation student, Rafael M. Petecof, master student, Samuel M. R. Noronha, Bsc, PhD, Silvana A. A. Correa, Bsc, PhD, Lydia M. Ferreira, Full Professor.
UNIVERSIDADE FEDERAL DE SÃO PAULO, São Paulo, Brazil.
Keloid is a dermal injury resulting from an abnormal healing process. The molecular mechanisms that lead to the formation of keloid and hypertrophic scars are poorly understood. The aim of the study was evaluate gene expression of 84 mediators of wound healing (WH) and oxidative stress (OS) by means of PCR array.
It was evaluated 12 patients with keloids and 12 patients underwent aesthetic surgery (control). The skin fragments of both groups were used for total RNA extraction and subsequent analysis by qPCR array in triplicate.
For WH, 46 genes (55%) were differentially expressed, 25 (54%) hiperegulated and 21 (46%) hyporegulated. The genes that showed greater differential were (in times): FGF10 (19), TNF (18), and MMP1 (15). For OS, 33 genes (39%) differentially expressed, 24 (73%) hiperegulated and 09 (27%) hyporegulated. The genes that showed greater differential was (in times): NOS2 (25), LPO (19), PTGS2 (13), SPINK1 (10), and MBL2 (15).
The healing process expressed predominantly high levels of FGF10 or KGF-2 that is expressed by fibroblasts and is a potent mitogenic inducing proliferation and migration of keratinocytes and secretion of metalloproteinases; and they were hiperexpressed in this study. MMP-1 plays a central role in the pathogenesis of abnormal collagen. LPO, NOS2, SPINK1 and PTGS2, respectively, produced changes that lead to increased production of free radicals, increased synthesis of collagen, cell proliferation, and the proliferation of extracellular matrix by keloid. Thus, the overexpression of these genes in this study corroborates with previous studies. Support: FAPESP 2013/10905-0
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