Abstract

Glycosylation is one of the most important post-translational modifications. It is clear that the single step of beta-1,4-galactosylation is performed by a family of beta-1,4-galactosyltransferases (beta-1,4-GalTs), and that each member of this family may play a distinct role in different tissues and cells. In the present study, real-time PCR revealed that the beta-1,4-GalT I mRNA reached peaks at 2 weeks after sciatic nerve crush and 3 days after sciatic nerve transection. Combined in situ hybridization for beta-1,4-GalT I mRNA and immunohistochemistry for S100 showed that beta-1,4-GalT I mRNAs were mainly located in Schwann cells after sciatic nerve injury. In conclusion, beta-1,4-GalT I might play important roles in Schwann cells during the regeneration and degeneration of the injured sciatic nerve. In other pathology, such as inflammation, we found that LPS administration affected beta-1,4-GalT I mRNA expression in sciatic nerve in a time- and dose-dependent manner, and beta-1,4-GalT I mRNA is expressed mainly in Schwann cells. These results indicated that beta-1,4-GalT I plays an important role in the inflammation reaction induced by intraperitoneal injection of LPS. Similarly, we found that beta-1,4-GalT I in Schwann cells in vitro was affected in a time- and concentration-dependent manner in response to LPS stimulation. All these results suggest that beta-1,4-GalT I play an important role in Schwann cells in vivo and vitro during pathology. In addition, beta-1,4-GalT I production was drastically suppressed by U0126 (ERK inhibitor), SB203580 (p38 inhibitor), or SP600125 (SAPK/JNK inhibitor), which indicated that Schwann cells which regulated beta-1,4-GalT I expression after LPS stimulation were via ERK, SAPK/JNK, and P38 MAP kinase signal pathways.

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