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Construction and Characterization of a Novel Vocal Fold Bioreactor
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TGFβ/Smad2/3-Mediated Crosstalk Between Vocal Fold Fibroblasts and Myoblasts In Vitro.

Masayoshi Yoshimatsu1, Ryosuke Nakamura1, Renjie Bing1

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Fibrotic vocal fold mucosa impairs muscle cell differentiation via TGF-β signaling. Muscle cells may reciprocally reduce fibrosis, suggesting a therapeutic target for vocal fold disorders.

Keywords:
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Area of Science:

  • Vocal fold (VF) physiology and pathology
  • Cellular and molecular biology
  • Fibrosis research

Background:

  • Vocal fold (VF) disorders traditionally separate mucosal and muscle issues.
  • Emerging evidence shows reciprocal interactions in other organs.
  • This study investigates potential crosstalk between VF mucosa and muscle.

Purpose of the Study:

  • To test the hypothesis that fibrotic vocal fold mucosa influences adjacent muscle.
  • To model the interaction between human vocal fold fibroblasts (HVOX) and rat vocal fold myoblasts (rVF-Mbs).
  • To explore reciprocal influences between these cell types.

Main Methods:

  • Human VF fibroblasts (HVOX) were stimulated with TGF-β1.
  • Effects on rat VF myoblasts (rVF-Mbs) were assessed via conditioned media and co-culture.
  • Myogenic differentiation, gene expression, and signaling pathways (Smad2/3, ALK4/5) were analyzed.

Main Results:

  • Fibrotic HVOX cells suppressed rVF-Mbs myogenic differentiation.
  • Co-culture showed greater inhibition than conditioned media, with reduced myotube formation and Myh2 expression.
  • Differentiating rVF-Mbs reduced the fibrogenic phenotype of HVOX fibroblasts.

Conclusions:

  • Fibrotic vocal fold mucosal cells impair muscle differentiation through TGF-β/Smad2/3 signaling.
  • Vocal fold muscle cells may exert reciprocal anti-fibrotic effects.
  • Mucosa-muscle interactions are implicated in VF pathology, with Smad2/3 as a potential therapeutic target.