OBJECTIVES: Inflammatory factors are key mediators of wound healing processes following injury, and their modulation may improve healing outcomes. The objective of this study was to characterize in vivo inflammatory factor and extracellular matrix (ECM) messenger RNA (mRNA) expression levels 1 hour after vocal fold injury. METHODS: Five Sprague-Dawley rats were subjected to bilateral vocal fold injury, 5 rats were reserved as uninjured controls, and 1 rat was subjected to unilateral vocal fold injury and reserved for histology. Tissue was harvested 1 hour after injury. Real-time reverse transcription-polymerase chain reaction was performed to examine the mRNA expression profiles of inflammatory factors nuclear factor kappa beta (NF-kappabeta), interferon gamma (IFN-gamma), cyclooxygenase 2 (COX-2), transforming growth factor beta isoform 1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta), as well as ECM genes hyaluronic acid synthase (HAS) 1, HAS-2, procollagen 1, procollagen 3, and elastin, in the injured samples compared with the uninjured controls. RESULTS: Injury resulted in subepithelial bleeding throughout the vocal fold. The COX-2, TNF-alpha, IL-1beta, and HAS-1 mRNA expression levels were significantly up-regulated 1 hour after injury compared with the uninjured controls. CONCLUSIONS: Inflammatory factor and ECM gene expression changes occur in vocal fold wound sites as early as 1 hour after injury. These results should inform future efforts to attenuate vocal fold scarring via the modulation of inflammatory factors.
OBJECTIVES: Inflammatory factors are key mediators of wound healing processes following injury, and their modulation may improve healing outcomes. The objective of this study was to characterize in vivo inflammatory factor and extracellular matrix (ECM) messenger RNA (mRNA) expression levels 1 hour after vocal fold injury. METHODS: Five Sprague-Dawley rats were subjected to bilateral vocal fold injury, 5 rats were reserved as uninjured controls, and 1 rat was subjected to unilateral vocal fold injury and reserved for histology. Tissue was harvested 1 hour after injury. Real-time reverse transcription-polymerase chain reaction was performed to examine the mRNA expression profiles of inflammatory factors nuclear factor kappa beta (NF-kappabeta), interferon gamma (IFN-gamma), cyclooxygenase 2 (COX-2), transforming growth factor beta isoform 1 (TGF-beta1), tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-1beta), as well as ECM genes hyaluronic acid synthase (HAS) 1, HAS-2, procollagen 1, procollagen 3, and elastin, in the injured samples compared with the uninjured controls. RESULTS: Injury resulted in subepithelial bleeding throughout the vocal fold. The COX-2, TNF-alpha, IL-1beta, and HAS-1 mRNA expression levels were significantly up-regulated 1 hour after injury compared with the uninjured controls. CONCLUSIONS: Inflammatory factor and ECM gene expression changes occur in vocal fold wound sites as early as 1 hour after injury. These results should inform future efforts to attenuate vocal fold scarring via the modulation of inflammatory factors.
Authors: Erik R Swanson; Tsunehisa Ohno; Dave Abdollahian; C Gaelyn Garrett; Bernard Rousseau Journal: Otolaryngol Head Neck Surg Date: 2010-10 Impact factor: 3.497