The Relationship Between Src-Suppressed C Kinase Substrate and β-1,4 Galactosyltransferase-I in the Process of Lipopolysaccharide-Induced TNF-α Secretion in Rat Primary Astrocytes

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.