Title of article :
Dynamic Biomechanical Strain Inhibits IL-1خ²â€“induced Inflammation in Vocal Fold Fibroblasts
Author/Authors :
Ryan C. Branski، نويسنده , , Priyangi Perera، نويسنده , , Katherine Verdolini، نويسنده , , Clark A. Rosen، M.D نويسنده , , Patricia A. Hebda، نويسنده , , Sudha Agarwal، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
Pages :
10
From page :
651
To page :
660
Abstract :
Despite the fact that vocal folds are subjected to extensive mechanical forces, the role of mechanical strain in vocal fold wound healing has been overlooked. Recent studies on other tissues have demonstrated that low physiological levels of mechanical forces are beneficial to injured tissues, reduce inflammation, and induce synthesis of matrix-associated proteins essential for enhanced wound healing. In this study, we speculated that mechanical strain of low magnitudes also attenuates the production of inflammatory mediators and alters the extracellular matrix synthesis to augment wound healing in cultured vocal fold fibroblasts. To test this hypothesis, fibroblasts from rabbit vocal folds were isolated and exposed to various magnitudes of cyclic tensile strain (CTS) in the presence or absence of interleukin-1خ² (IL-1خ²). Results suggest that IL-1خ² activates proinflammatory gene transcription in vocal fold fibroblasts. Furthermore, CTS abrogates the IL-1خ²â€“induced proinflammatory gene induction in a magnitude-dependent manner. In addition, CTS blocks IL-1خ²â€“mediated inhibition of collagen type I synthesis, and thereby upregulates collagen synthesis in the presence of IL-1خ². These findings are the first to reveal the potential utility of low levels of mechanical signals in vocal fold wound healing, and support the emerging on vivo data suggesting beneficial effects of vocal exercise on acute phonotrauma.
Keywords :
Vocal fold fibroblasts , inflammation , Interleukin-1خ² , Dynamic mechanical strain
Journal title :
Journal of Voice
Serial Year :
2007
Journal title :
Journal of Voice
Record number :
1280346
Link To Document :
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