Journal
CELLULAR AND MOLECULAR NEUROBIOLOGY
Volume 31, Issue 7, Pages 1047-1056Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-011-9704-3
Keywords
SSeCKS; beta-1,4 Galactosyltransferase-I; Astrocytes; Lipopolysaccharide
Categories
Funding
- National Natural Science Foundation of China [30770488, 30870320, 31070723, 81070275]
- Natural Science Foundation of Jiangsu Province [BK2009156, BK2009157, BK2009161, BK2010 169]
- Jiangsu Higher Education Institutions (PAPD)
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Src-suppressed C kinase substrate (SSeCKS), a protein kinase C substrate, is a major lipopolysaccharide (LPS) response protein. In addition, beta-1,4 Galactosyltransferase-I (beta-1,4-GalT-I) also plays an important role in the inflammation reactions of nervous system. It was reported that both SSeCKS and beta-1,4-GalT-I were involved in the LPS-induced tumor necrosis factor-alpha (TNF-alpha) expression in rat primary astrocytes. However, the functional interaction between SSeCKS and beta-1,4-GalT-I in the LPS-induced TNF-alpha secretion remains unclear. Therefore, in this study, using the inflammation model of astrocytes treated by LPS in vitro, we found that the changed expressions of SSeCKS and beta-1,4-GalT-I participated in LPS-induced TNF-alpha secretion through p38, JNK, and ERK signal transduction pathways in rat primary astrocytes. Knockdown by small-interfering RNAs (siRNAs) or overexpression of SSeCKS and beta-1,4-GalT-I could influence Mitogen-activated protein kinases (MAPKs) signaling pathways activation and TNF-alpha secretion. Besides, we confirmed that knockdown of SSeCKS could prevent the induction of beta-1,4-GalT-I in this process. Inversely, beta-1,4-GalT-I had no significant effect on SSeCKS expression in the same way. In summary, our data indicated that SSeCKS could regulate LPS-induced TNF-alpha secretion through beta-1,4-GalT-I in rat primary astrocytes.
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