Expression change of β-1,4 galactosyltransferase I, V mRNAs and Galβ1,4GlcNAc group in rat sciatic nerve after crush
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. beta-1,4-GalT I and V are involved in the biosynthesis of N-linked oligosaccharides. In the present study, Real-time PCR revealed that the beta-1,4-GalT I and V mRNAs reached peaks at 2 w after sciatic nerve crush. In situ hybridization showed that at 1 d after sciatic nerve crush, the expression levels of beta-1,4-GalT I and V mRNAs were strong at the crush site, and decreased gradually from crush site to the distal segments. In addition, combined in situ hybridization for beta1,4-GalT I and V mRNAs and immunohistochemistry for S100 showed that beta1,4-GalT I and V mRNAs were mainly located in Schwann cells. Lectin blot showed that the expression of Galbeta1,4GlcNAc group increased at 6 h immediately, reached a peak at 12 h and remained elevated up to 4 w after sciatic nerve crush. In conclusion, beta1,4-GalT I and V might play important roles in the regeneration of the injured sciatic nerve, and upregulation of Galbeta1,4GlcNAc group might be correlated with the process of the sciatic nerve injury.
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- "It has also been shown that the significant delay of skin-wound healing is concomitant with reduced leukocyte infiltration at the wound site in b-1,4-GalT-I-deficient mice (Mori et al., 2004). Our previous study reported that b-1,4-GalT-I and -V may play important roles in the regeneration of injured sciatic nerve (Yan et al., 2008). We also revealed that b-1,4-GalT-I is a key inflammation mediator in the initiation and maintenance of inflammatory reactions in spinal cord injury (SCI; Niu et al., 2008). "
ABSTRACT: Pyrroloquinoline quinone (PQQ) is a water-soluble, anionic, quinonoid substance that has been established as an essential nutrient in animals. Owing to the inherent properties of PQQ as an antioxidant and redox modulator in various systems, PQQ is expected to be used in pharmacological applications in the near future. Although many recent studies have investigated its neuroprotective effects, the effect of PQQ on traumatic brain injury (TBI) has not been examined. In this study we employed Morris water maze (MWM) training, the results of which showed that PQQ led to improved behavioral performance in post-TBI animals. Considering that many experiments have suggested that β-1,4-galactosyltransferase I (β-1,4-GalT-I) and -V play significant roles in inflammation and the nervous system, in the present study we used Western blot analysis to study the effect of PQQ on the expression of β-1,4-GalT-I and -V. We found apparent expression upregulation of β-1,4-GalT-I and -V after PQQ was systemically administered. Lectin-fluorescent staining with RCA-I also revealed that PQQ contributed to expression upregulation of the galactosidase β-1 (Gal β-1), 4-galactosyltransferase N-acylsphingosine (4-GlcNAc) group in microglia and neurons of the cortex and hippocampal CA2 region. In summary, our experiment established that PQQ may play an important role in recovery post-TBI.Journal of neurotrauma 12/2011; 29(5):851-64. DOI:10.1089/neu.2011.1882
- Journal of Molecular Histology 08/2008; 39(4). DOI:10.1007/s10735-008-9182-1
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ABSTRACT: beta4 Galactosylation of glycoproteins is one of the most important post-translational modifications. Recent studies have demonstrated that aberrant galactosylation associates with some inflammation diseases. beta-1,4-galactosyltransferase-I (beta-1,4-GalT-I), which transfers galactose to the terminal N-acetylglucosamine of N- and O-linked glycans in a beta-1,4- linkage, considered to be the major galactosyltransferse among the seven members of the subfamily responsible for beta4 galactosylation. In the present study, we investigated the expression of beta-1,4-GalT-I in Schwann cells under Lipopolysaccharide (LPS) treatment. RT-PCR revealed that the beta-1,4-GalT-I mRNA was significant increased as early as 2 h after LPS stimulation. Immunofluorescence showed that beta-1,4-GalT-I was located in Golgi apparatus and membrane of Schwann cells. With the 1 microg/ml LPS treatment, expression levels of beta-1,4-GalT-I was much higher compared with control group. In addition, lectin blot indicated that the beta4 galactosylation of glycoproteins such as integrin alpha5 was enhanced, which may due to the induced beta-1,4-GalT-I expression. These results suggested that beta-1,4-GalT-I may play an important role in adhesion and migration of Schwann cells during inflammation.Inflammation 07/2009; 32(5):279-86. DOI:10.1007/s10753-009-9131-5