The effect of silk-gelatin bioink and TGF-β3 on mesenchymal stromal cells in 3D bioprinted chondrogenic constructs: A proteomic study

Major limitation of 3D bioprinting is the poor understanding of the role of bioink in modulating molecular signaling pathways. Phenotypically stable engineered articular cartilage was fabricated using silk fibroin-gelatin (SF-G) bioink and progenitor cells or mature articular chondrocytes. In the current study, role of SF-G bioink in modulating in vitro chondrogenic signaling pathways in human bone marrow-derived stromal cells (hMSCs) is elucidated. The interaction between SF-G bioink and hMSCs augmented several chondrogenic pathways, including Wnt, HIF-1, and Notch. We explored the debatable role of TGF-beta signaling, by assessing the differential protein expression by hMSCs-laden bioprinted constructs in the presence and absence of TGF-beta 3. hMSCs-laden bioprinted constructs contained a large percentage of collagen type II and Filamin-B, typical to the native articular cartilage. Hypertrophy markers were not identified following TGF-beta 3 addition. This is first detailed proteomics analysis to identify articular cartilage-specific pathways in SF-G-based 3D bioprinted construct.

Automated summary

One major limitation of 3D bioprinting is the lack of understanding of the role of bioink in modulating molecular signaling pathways. The interaction between SF-G bioink and hMSCs enhanced several chondrogenic pathways, providing potential for further research in this area. This study represents the first detailed proteomics analysis to identify articular cartilage-specific pathways in SF-G-based 3D bioprinted constructs.