Table 1.
Primer sequences for target genes.
Fig 1.
Gene expression of HYAL1 comparing A) timepoints after nerve crush injury and B) comparing nerve injury models at 3 weeks after injury (n = 6). Gene expression data show an overall downregulation of HYAL1 after injury with the greatest expression at 3 weeks after crush injury. Significant differences are observed between injury models, with transection exhibiting the greatest downregulation at 3 weeks. Protein expression of HYAL1 quantified through immunohistochemical analysis across C) timepoints after nerve crush injury and D) nerve injury models 3 weeks after injury (n = 3). There appear to be no differences in protein expression between timepoints or injury models. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.
Fig 2.
Gene expression of HYAL2 comparing A) timepoints after nerve crush injury and B) comparing nerve injury models 3 weeks after injury (n = 6). Temporal changes are observed following nerve crush with the greatest expression between 3 days and 1 week. No significant differences in gene expression are observed between injury models at 3 weeks. Protein expression of HYAL2 quantified through immunohistochemical analysis comparing C) timepoints after nerve crush injury and D) comparing nerve injury models 3 weeks after injury (n = 3). No significant differences observed between crush timepoints or injury models. * p<0.05, ** p<0.01, *** p<0.001.
Fig 3.
Gene expression of CD44 comparing A) timepoints after nerve crush injury and B) comparing nerve injury models at 3 weeks after injury (n = 6). There appear to be temporal changes after nerve crush with the greatest CD44 gene expression observed at 3 days after crush. Between injury models at 3 weeks, CD44 is highly expressed following transection at 3 weeks compared to other groups. HA quantification comparing C) timepoints after nerve crush injury and D) comparing nerve injury models 3 weeks after injury (n = 6). No differences observed in HA concentration between crush timepoints, while there is a significantly lower HA concentration measured after transection at 3 weeks. # = not significant to fresh tissue, ^ p<0.0001 to 1 day and 3 day, * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001.
Fig 4.
Gene array analysis of various ECM proteins, proteases, and adhesion molecules after nerve injury (n = 1, no statistical power).
Overlay of ECM proteases with A) protease inhibitors and B) ECM molecules including collagens, structural constituents, and cell adhesion molecules. Temporal patterns of C) matrix metalloproteases (mmps) and D) tissue inhibitors of metalloproteinases (timps) after nerve crush show differences in patterning across different molecular species. Comparison of fold regulation compared to Fresh tissue of E) mmps and F) timps 3 weeks after crush versus transection show differences between injury models.
Fig 5.
Comparison of hyaluronidase activity following A) nerve crush injury at various timepoints and B) 3 weeks after nerve crush vs. transection injury (n = 6). No significant differences observed between crush timepoints or injury models. Hyaluronidase specific activity measurements comparing A) nerve crush injury at various timepoints and B) 3 weeks after crush and transection injuries (n = 6). No differences in specific activity observed between crush timepoints, although there appears to be a greater specific activity after transection, related to a higher matrix turnover. ** p< 0.01, *** p<0.001.