Journal
JOURNAL OF VOICE
Volume 21, Issue 6, Pages 651-660Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jvoice.2006.06.005
Keywords
vocal fold fibroblasts; inflammation; Interleukin-1 beta; dynamic mechanical strain
Funding
- NCCIH NIH HHS [AT00646, R01 AT000646] Funding Source: Medline
- NIDCD NIH HHS [R01 DC005643, F31 DC06764-01, DC5643] Funding Source: Medline
- NIDCR NIH HHS [R01 DE015399] Funding Source: Medline
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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-1 beta (IL-1 beta). Results suggest that IL-1 beta activates proinflammatory gene transcription in vocal fold fibroblasts. Furthermore, CTS abrogates the IL-1 beta-induced proinflammatory gene induction in a magnitude-dependent manner. In addition, CTS blocks IL-1 beta-mediated inhibition of collagen type I synthesis, and thereby upregulates collagen synthesis in the presence of IL-1 beta. 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.
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