TY - JOUR
T1 - Immediate inflammatory response and scar formation in wounded vocal folds
AU - Lim, Xinhong
AU - Tateya, Ichiro
AU - Tateya, Tomoko
AU - Muñoz-Del-Río, Alejandro
AU - Bless, Diane M.
N1 - Funding Information:
From the Division of Otolaryngology-Head and Neck Surgery, University of Wisconsin-Madison, Madison, Wisconsin. This study was supported by grant R01DC4428 from the National Institutes of Health/National Institute on Deafness and Other Communication Disorders. This study was performed in accordance with the PHS Policy on Humane Care and Use of Laboratory Animals, the NIH Guide for the Care and Use of Laboratory Animals, and the Animal Welfare Act (7 U.S.C. et seq.); the animal use protocol was approved by the Institutional Animal Care and Use Committee (IACUC) of the University of Wisconsin-Madison.
PY - 2006/12
Y1 - 2006/12
N2 - Objectives: Vocal fold scarring is the major cause of voice disorders after voice surgery or laryngeal trauma. The role of inflammatory factors in vocal fold wound healing and fibrosis has not been adequately investigated. Scarless wound healing has been associated with decreased inflammatory responses. To understand scar formation and develop reliable treatments, it is necessary to control extracellular matrix production and inflammation. Thus, we examined the inflammation profile and extracellular matrix production in wounded vocal folds in the acute phase of wound healing. Methods: Vocal fold stripping was performed on 30 Sprague-Dawley rats. Vocal fold tissue was collected at 5 time points (4, 8, 16, 24, and 72 hours). We examined the in vivo messenger RNA expression profile of inflammatory factors interleukin 1β, interferon γ, tumor necrosis factor a, nuclear factor κβ, transforming growth factor β, and cyclooxygenase 2, as well as hyaluronic acid synthases 1 and 2, procollagen subtypes I and III, and elastin synthase in scarred vocal folds after injury, compared to normal vocal folds, using real-time reverse transcription-polymerase chain reaction. Results: The inflammatory factors showed a time-dependent sequence of expression peaks, starting with interleukin 1β, nuclear factor κβ, tumor necrosis factor α (4 and 8 hours), and transforming growth factor β (72 hours). Interferon γ decreased at 24 hours. Correspondingly, hyaluronic acid synthase 1 expression peaked first (4 and 8 hours), whereas hyaluronic acid synthase 2 expression peaked at 16 hours and again at 72 hours. Procollagen I expression peaked at 72 hours, whereas procollagen III decreased from 8 to 16 hours but peaked at 72 hours. Cyclooxygenase 2 expression was elevated, whereas elastin expression remained constant. Conclusions: The results show a clear profile of vocal fold inflammation with corresponding changes in extracellular matrix production.
AB - Objectives: Vocal fold scarring is the major cause of voice disorders after voice surgery or laryngeal trauma. The role of inflammatory factors in vocal fold wound healing and fibrosis has not been adequately investigated. Scarless wound healing has been associated with decreased inflammatory responses. To understand scar formation and develop reliable treatments, it is necessary to control extracellular matrix production and inflammation. Thus, we examined the inflammation profile and extracellular matrix production in wounded vocal folds in the acute phase of wound healing. Methods: Vocal fold stripping was performed on 30 Sprague-Dawley rats. Vocal fold tissue was collected at 5 time points (4, 8, 16, 24, and 72 hours). We examined the in vivo messenger RNA expression profile of inflammatory factors interleukin 1β, interferon γ, tumor necrosis factor a, nuclear factor κβ, transforming growth factor β, and cyclooxygenase 2, as well as hyaluronic acid synthases 1 and 2, procollagen subtypes I and III, and elastin synthase in scarred vocal folds after injury, compared to normal vocal folds, using real-time reverse transcription-polymerase chain reaction. Results: The inflammatory factors showed a time-dependent sequence of expression peaks, starting with interleukin 1β, nuclear factor κβ, tumor necrosis factor α (4 and 8 hours), and transforming growth factor β (72 hours). Interferon γ decreased at 24 hours. Correspondingly, hyaluronic acid synthase 1 expression peaked first (4 and 8 hours), whereas hyaluronic acid synthase 2 expression peaked at 16 hours and again at 72 hours. Procollagen I expression peaked at 72 hours, whereas procollagen III decreased from 8 to 16 hours but peaked at 72 hours. Cyclooxygenase 2 expression was elevated, whereas elastin expression remained constant. Conclusions: The results show a clear profile of vocal fold inflammation with corresponding changes in extracellular matrix production.
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U2 - 10.1177/000348940611501212
DO - 10.1177/000348940611501212
M3 - Article
C2 - 17214268
AN - SCOPUS:33846149640
SN - 0003-4894
VL - 115
SP - 921
EP - 929
JO - Annals of Otology, Rhinology and Laryngology
JF - Annals of Otology, Rhinology and Laryngology
IS - 12
ER -