Covalent binding of placental derived proteins to silk fibroin improves schwann cell adhesion and proliferation

Schuh, Christina M. A. P.; Monforte, Xavier; Hackethal, Johannes; Redl, Heinz; Teuschl, Andreas H.

Abstract

Schwann cells play a key role in peripheral nerve regeneration. Failure in sufficient formation of Bungner bands due to impaired Schwann cell proliferation has significant effects on the functional outcome after regeneration. Therefore, the growth substrate for Schwann cells should be considered with highest priority in any peripheral nerve tissue engineering approach. Due to its excellent bio-compatibility silk fibroin has most recently attracted considerable interest as a biomaterial for use as conduit material in peripheral nerve regeneration. In this study we established a protocol to covalently bind collagen and laminin, which have been isolated from human placenta, to silk fibroin utilizing carbodiimide chemistry. Altered adhesion, viability and proliferation of Schwann cells were evaluated. A cell adhesion assay revealed that the functionalization with both, laminin or collagen, significantly improved Schwann cell adhesion to silk fibroin. Moreover laminin drastically accelerated adhesion. Schwann cell proliferation and viability assessed with BrdU and MTT assay, respectively, were significantly increased in the laminin-functionalized groups. The results suggest beneficial effects of laminin on both, cell adhesion as well as proliferative behaviour of Schwann cells. To conclude, the covalent tailoring of silk fibroin drastically enhances its properties as a cell substratum for Schwann cells, which might help to overcome current hurdles bridging long distance gaps in peripheral nerve injuries with the use of silk-based nerve guidance conduits.

Más información

Título según WOS: ID WOS:000388631200015 Not found in local WOS DB
Título de la Revista: JOURNAL OF MATERIALS SCIENCE-MATERIALS IN MEDICINE
Volumen: 27
Número: 12
Editorial: Springer
Fecha de publicación: 2016
DOI:

10.1007/s10856-016-5783-5

Notas: ISI