ArticleThe Laryngoscope2017
Cellular source and proinflammatory roles of high-mobility group box 1 in surgically injured rat vocal folds.
Article in The Laryngoscope, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A Human Vocal Fold Organ-On-Chip for Studying Platform-Dependent Mucosal Responses to Particulate Matter.bioRxiv : the preprint server for biology · 2026Article
- Preclinical Vocal Fold and Airway Injury Models: A Scoping Review.Laryngoscope investigative otolaryngology · 2025Review
- Controlled decorin delivery from injectable microgels promotes scarless vocal fold repair.bioRxiv : the preprint server for biology · 2025Article
- Progress in Vocal Fold Regenerative Biomaterials: An Immunological Perspective.Advanced nanobiomed research · 2022Article
- An in vitro assessment of the response of THP-1 macrophages to varying stiffness of a glycol-chitosan hydrogel for vocal fold tissue engineering applications.Journal of biomedical materials research. Part A · 2021Article
- In vitro mechanical vibration down-regulates pro-inflammatory and pro-fibrotic signaling in human vocal fold fibroblasts.PloS one · 2020Article
- Towards a Physiological Scale of Vocal Fold Agent-Based Models of Surgical Injury and Repair: Sensitivity Analysis, Calibration and Verification.Applied sciences (Basel, Switzerland) · 2019Article
- A paper-based microfluidic platform with shape-memory-polymer-actuated fluid valves for automated multi-step immunoassays.Microsystems & nanoengineering · 2019Article
- High-Performance Agent-Based Modeling Applied to Vocal Fold Inflammation and Repair.Frontiers in physiology · 2018Article
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Authors and funding
5 authors.
Funding
Abstract
objectives/hypothesisHigh-mobility group box 1 (HMGB1) is a chromatin-binding protein located in the cell nucleus. Following injury, immunocompetent cells secrete HMGB1 to the extracellular milieu under the stimulation of proinflammatory cytokines. Extracellular HMGB1 acts a danger signal that instigates the innate immunity and tissue repair. We previously reported HMGB1 in the vocal fold extracellular compartment between day 3 and day 7 following surgical injury. In this study, we further investigated the cell source of HMGB1 and the relationship of proinflammatory cytokine expression and HMGB1 translocation in wounded vocal folds. STUDY
designProspective animal study.
methodsBilateral vocal fold injury was performed on 122 Sprague-Dawley rats. An additional 18 rats served as uninjured controls. Animals were sacrificed at multiple time points up to 4 weeks after surgery. Immunohistochemical costaining was performed to identify the cell source of HMGB1. Cell markers ED1, fibroblast-specific protein 1 (FSP1), and alpha smooth muscle actin (α-SMA) were used to identify macrophages, fibroblasts, and myofibroblasts, respectively. Enzyme-linked immunosorbent assays were performed to measure cytokine levels of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in vocal fold tissue.
resultsCostaining of HMGB1 was strong with ED1 and FSP1 but was minimal with α-SMA in injured vocal folds. Compared to uninjured controls, IL-1β and TNF-α expression increased significantly the first 2 days after injury.
conclusionsMacrophages and fibroblasts were a major cell source of vocal fold HMGB1. Translocation of HMGB1 may be an active response to the early accumulation of IL-1β and TNF-α in the wounded vocal folds. LEVEL OF EVIDENCE: NA Laryngoscope, 127:E193-E200, 2017.
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