# Accelerated peripheral nerve repair using surface-modified biomaterials for targeted capture of glial-derived growth factors post-neurorrhaphy

**Authors:** Shiu-Jau Chen, Chih-Ming Lin, Chiung-Hui Liu, Yin-Hsiu Chen, Yu-Lin Hsieh, You-Cheng Lin, Yin-Hung Chu, Chung-Yao Ku, Wei-Li Liao, Wen-Chieh Liao

PMC · DOI: 10.1371/journal.pone.0319979 · PLOS One · 2025-04-11

## TL;DR

This study explores how modifying biomaterials with syndecan-3 can improve nerve repair by capturing growth factors and boosting cell growth.

## Contribution

The novel contribution is the use of syndecan-3-modified SIS to enhance growth factor retention and accelerate nerve regeneration.

## Key findings

- SDC3-coated SIS significantly enhanced Schwann cell proliferation and neurite outgrowth in vitro.
- One month post-surgery, the GDNF+SDC3-coated SIS group showed a 1.6-fold increase in β3-tubulin-positive axons.
- CMAP amplitude increased in the GDNF+SDC3 group, indicating improved motor axon function in rats.

## Abstract

Peripheral nerve injury (PNI) commonly leads to motor or sensory dysfunction, with nerve grafts being the standard treatment for neurorrhaphy. Despite advancements in biomaterials for nerve-tissue engineering, the rate of nerve regeneration remains slow. Therefore, this study aims to improve further the understanding of the impact of syndecan-3 (SDC3)-modified small intestine submucosa (SIS) on nerve reconstruction by employing two advanced approaches: cation recruitment and local growth factor delivery. Immunofluorescence staining confirmed the presence of SDC3 conjugated on the SIS. The enzyme-linked immunosorbent assay measured sustained glial cell line-derived neurotrophic factor (GDNF) levels in the SDC3-coated SIS. In vitro studies showed that SDC3-coated SIS retained GDNF in a dose-dependent manner, significantly enhancing Schwann cell proliferation compared with basal conditions. RSC96 cells proliferated most effectively on SDC3-coated SIS loaded with GDNF, and neuro-2A neurites were significantly longer on this material at 48 hours. One-month post-neurorrhaphy, morphological analysis revealed a 1.6 ±  0.02-fold increase in the number of β3-tubulin-positive axons in the GDNF+SDC3-coated SIS group compared to the SIS group. CMAP amplitude increases in the GDNF+SDC3-coated SIS group as more functioning motor axons are connected to the target muscle of ESN rats. This study provides valuable insights into the development of customized SDC3-coated SIS for promoting nerve tissue regeneration and accelerating rehabilitation.

## Linked entities

- **Genes:** SDC3 (syndecan 3) [NCBI Gene 9672]
- **Proteins:** GDNF (glial cell derived neurotrophic factor)

## Full-text entities

- **Genes:** Sdc3 (syndecan 3) [NCBI Gene 116673], Gdnf (glial cell derived neurotrophic factor) [NCBI Gene 25453] {aka gndf}
- **Diseases:** motor or sensory dysfunction (MESH:C536988), PNI (MESH:D059348)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]
- **Cell lines:** neuro- — Mus musculus (Mouse), Mouse neuroblastoma, Cancer cell line (CVCL_0470), RSC96 — Rattus norvegicus (Rat), Spontaneously immortalized cell line (CVCL_4694)

## Full text

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## Figures

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## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC11990746/full.md

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Source: https://tomesphere.com/paper/PMC11990746