The data suggest that VFE produces significant improvement in subjective, objective, and patient self-evaluation and deserves further attention as a treatment for aged atrophy of the vocal fold. It was also suggested that VFE does not improve the vocal fold bowing but may improve muscular function during voicing.
Objectives/Hypothesis
Mesenchymal stem cells (MSCs) hold therapeutic promise for vocal fold scar, yet the precise mechanism(s) underlying tissue level changes remain unclear. We hypothesize that MSCs interact with native fibroblasts to favorably affect healing. Furthermore, we hypothesize these interactions vary based on MSC source.
Methods
Vocal fold fibroblasts (VFFs), adipose-derived stem cells (ASCs), and bone-marrow derived stem cells (BMSCs) were extracted from Sprague-Dawley rats and a co-culture model was employed culturing VFFs+/-TGF-β1 (10ng/ml) +/− MSCs. Mono-culture MSCs were also prepared as a control. Both extracellular matrix (ECM) and components of the TGF-β signaling pathway were analyzed via polymerase chain reaction and SDS-PAGE.
Results
Significantly decreased TGF-β1 mRNA and α-smooth muscle actin protein was observed in VFFs in response to TGF-β1 in the co-culture with both MSCs (p<0.05, p<0.01). BMSCs significantly downregulated Collagen I (p<0.05), Collagen III (p<0.05), Smad3 (p<0.01), and TGF-β1 receptor I (p<0.01) mRNA in VFFs. Hyaluronic synthase-1 and 2 increased in co-cultured BMSCs when compared with mono-cultured BMSCs at baseline and in response to TGF-β1 (p<0.01).
Conclusions
MSCs had a favorable effect on ECM regulation as well as suppression of TGF-β1 signaling in VFF. Bidirectional paracrine signaling was also observed as VFFs altered ECM regulation in MSCs. These data provide insight into the regenerative effects of MSCs and provide a foundation for clinical application.
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