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Tracing Gene Expression Through Detection of β-galactosidase Activity in Whole Mouse Embryos
Published on: June 26, 2018
Expression of beta-1,4-galactosyltransferase I in rat Schwann cells
Huiguang Yang1, Meijuan Yan, Chun Cheng
1Department of Orthopaedics, Affiliated Jiangying Hospital of Nantong University, The Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong, Jiangsu Province 226001, P.R. China.
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.

