Expression data from rat vocal fold at different periods after vocal fold injury
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ABSTRACT:
PROVIDER: PRJNA579528 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from rat vocal fold at different periods after vocal fold injury (miRNA)
| PRJNA614953 | ENA
Project description:Vocal cord healing is a dynamic process, and many genes and proteins are involved, which play varying roles at different regeneration stages after injury. Previous studies have shown that inflammatory responses occur at the early stage of vocal cord injury, where the fibroblasts proliferate exuberantly with intensive secretion and deposition of ECM. These activities reach the peak at 3-7 days and their intensity begins to decline 15 days later. A study based on the dermal system has shown that ECM remodeling during the repair of injury can last for several months. However, few studies have been conducted as to the dynamic changes of gene expressions and signaling pathway during the healing process of vocal cord injury. Plotting these changes will facilitate the understanding about the physiological changes during healing and the identification of key time points and target genes in fibrosis formation.
2019-10-26 | GSE139383 | GEO
Project description:Vocal cord healing is a dynamic process, and many genes and proteins are involved, which play varying roles at different regeneration stages after injury. Previous studies have shown that inflammatory responses occur at the early stage of vocal cord injury, where the fibroblasts proliferate exuberantly with intensive secretion and deposition of ECM. These activities reach the peak at 3-7 days and their intensity begins to decline 15 days later. A study based on the dermal system has shown that ECM remodeling during the repair of injury can last for several months. However, few studies have been conducted as to the dynamic changes of gene and microRNA expressions during the healing process of vocal cord injury. Plotting these changes will facilitate the understanding about the physiological changes during healing and the identification of key time points and target genes and microRNAs in fibrosis formation.
2020-03-25 | GSE147473 | GEO
Project description:We used microarrays to characterize transcriptome profiles of rat vocal fold tissue following surgical injury (vs. naive tissue); rat vocal fold fibroblasts harvested from scar tissue at the 60 d time point (vs. naive fibroblasts); rat vocal fold scar fibroblasts treated with siRNA against the collagen chaperone protein rat gp46 (vs. scramble siRNA). Adult Fischer 344 rat vocal fold tissue was harvested at 3, 14, and 60 days following surgical injury (control = age-matched naive tissue); rat vocal fold scar fibroblasts were obtained via explant culture of tissue obtained 60 days following surgical injury and harvested at 80% confluence during passage 1 (control = age-matched naive rat vocal fold fibroblasts); rat vocal fold scar fibroblasts were treated for 1 h with 50 nM liposome-delivered siRNA against rat gp46 when 80% confluent at passage 1, cultured for an additional 24 h in fresh media, then harvested (control = rat vocal fold scar fibroblasts treated with 50 nM liposome-delivered scramble siRNA).
2014-10-09 | E-GEOD-62204 | biostudies-arrayexpress
Project description:We used microarrays to characterize transcriptome profiles of rat vocal fold tissue following surgical injury (vs. naive tissue); rat vocal fold fibroblasts harvested from scar tissue at the 60 d time point (vs. naive fibroblasts); rat vocal fold scar fibroblasts treated with siRNA against the collagen chaperone protein rat gp46 (vs. scramble siRNA).
2014-10-09 | GSE62204 | GEO
Project description:Vocal fold (VF) fibrosis, often caused by phonosurgery, radiation, or trauma, leads to irreversible voice dysfunction due to excessive ECM deposition and increased tissue stiffness. VF fibrosis, a significant cause of chronic dysphonia, lacks FDA-approved treatments, highlighting the critical need for novel antifibrotic therapeutic. TGF-β1 is a major driver in the pathological transformation of fibroblasts into contractile myofibroblasts in VF fibrosis via SMAD3, YAP1, and integrin signaling pathways. These pathways lead to increased ACTA2 expression, excessive collagen production, and progressive tissue stiffening. Leveraging the principle that local cells respond to tissue-specific signals, our ECM hydrogel derived from decellularized vocal fold lamina propria (VFLP-ECM) reduced ACTA2 expression in TGF-β1 stimulated vocal fold fibroblasts, showcasing antifibrotic potential. In this study, we evaluated the therapeutic potential of VFLP-ECM hydrogel in a rabbit VF injury model—treatment involved VFLP-ECM or bovine type I collagen injections into VFs 7 days after injury, with evaluations at 28 days post-injury. We compared two VFLP-ECM formulations: a manual process (VFLP (man)) and an accelerated automated method (VFLP (au)). VFLP (man) showed more modulated fibrosis-associated gene expressions when compared to VFLP (au) and collagen. Proteomic analysis revealed that VFLP (man) preserves a broader array of bioactive proteins, such as vitronectin, crucial in TGF-β1 signaling and ECM remodeling. The transcriptomic analysis uncovered a downregulation of key fibrotic markers and potential inhibition of regulators such as SMAD3, YAP1, and MRTFA, alongside the upregulation of SMAD7, an inhibitor of TGF-β signaling. Notably, treatment with VFLP (man) resulted in vocal folds with similar stiffness as uninjured controls, whereas tissues treated with collagen or VFLP (au) remained stiffer, indicating incomplete mechanical recovery. These data provide the first in vivo evidence that VFLP-ECM hydrogel—mainly when produced via manual decellularization—attenuates fibrosis by disrupting biochemical and biomechanical drivers of myofibroblast activation.
2025-07-29 | GSE295627 | GEO
Project description:Injection of Vocal Fold Lamina Propria-Derived Hydrogels Modulates Fibrosis in Injured Vocal Folds
| PRJNA1255487 | ENA
Project description:The purpose of this study is to investigate if acute systemic dehydration impacts the vocal folds at the mRNA level. Rabbits were used as animal model to enable a systematic and rigorous assessment of the pathobiology of vocal fold hydration since they can be manipulated in a physiologically realistic manner. We anticipate that the results of this study will help to elucidate the effects of altered hydration state in response to furosemide on vocal fold epithelium, lamina propria and muscle tissue at the transcriptome level. Together with cellular, structural, and functional techniques that are part of this project, we expect to provide validated scientific recommendations on the adverse effects of dehydration and the therapeutic benefits of hydration.
2020-07-09 | GSE132765 | GEO
Project description:We present here the first study evaluating the dynamic proteome changes in the remodeling process of decellularized tissue by reseeded cells using vocal fold mucosa as the model system.
2016-01-06 | PXD002734 | Pride
Project description:Increased extracellular matrix (ECM) and matrix stiffness promote solid tumor progression. However, mechanotransduction in cancers arising in mechanically active tissues remains underexplored. Here, we report upregulation of multiple ECM components accompanied by tissue stiffening in vocal fold cancer (VFC). We compare non-cancerous (NC) and patient-derived VFC cells – from early (mobile, T1) to advanced-stage (immobile, T3) cancers – revealing an association between VFC progression and cell-surface receptor heterogeneity, reduced laminin-binding integrin cell-cell junction localization and a flocking mode of collective cell motility. Mimicking physiological movement of healthy vocal fold tissue (stretching /vibration), decreases oncogenic nuclear β-catenin and YAP levels in VFC. Multiplex immunohistochemistry of VFC tumors uncovered a correlation between ECM content, nuclear YAP and patient survival, concordant with VFC sensitivity to YAP-TEAD inhibitors in vitro and in vivo. Our findings present evidence that VFC is a mechanically sensitive malignancy and restoration of tumor mechanophenotype or YAP/TAZ targeting, represents a tractable anti-oncogenic therapeutic avenue for VFC.
2025-11-25 | GSE297099 | GEO