The Effects of Botulinum Toxin Type A on the Biological Behavior of Fibroblasts on Silicone Implants

BackgroundCapsular contracture is one of the most severe complications following breast augmentation surgery. It has been reported that botulinum toxin Type A (BTX-A) can inhibit capsular contracture, but the exact mechanisms remain unclear. Therefore, this study aims to explore the potential mechanisms behind BTX-A's inhibition of capsular contracture by observing its effects on the biological behavior of fibroblasts and its impact on the TGF-beta/Smad signaling pathway.MethodsIn vitro experiments involved culturing fibroblasts on PDMS surfaces, subsequently treating them with various concentrations of BTX-A. Fibroblast proliferation activity was assessed using the CCK-8 assay, while the migration and cytoskeletal morphology of the fibroblasts were meticulously examined. ELISA was utilized to quantify the expression of fibrosis-related cytokines. Gene and protein expressions related to the TGF-beta/Smad pathway were analyzed through real-time PCR and Western blotting techniques.ResultsBTX-A moderately enhanced the early proliferation and migration of fibroblasts on the surface of PDMS silicone sheets and reduced the synthesis of collagen types I and III. Furthermore, under the influence of BTX-A, the expression of TGF-beta R2 and alpha-SMA in the TGF-beta/Smad pathway was significantly inhibited.ConclusionsThis study demonstrates that BTX-A can inhibit fibroblast differentiation by downregulating the expression of TGF-beta R2, thereby suppressing the TGF-beta/Smad pathway. This suggests a possible mechanism through which BTX-A mitigates capsular contracture.No Level AssignedThis journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266.