The role of TNF-α and its receptors in the production of Src-suppressed C kinase substrate by rat primary type-2 astrocytes

Yan, Ming; Xia, Chunlin; Cheng, Chun; Shao, Xiaorong; Niu, Shuqiong; Liu, Haiou; Shen, Aiguo

doi:10.1016/j.brainres.2007.09.082

Cited by 16 publications

(15 citation statements)

References 21 publications

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“…Our previous data indicated SSeCKS played a regulatory role in the cytokine production during inflammatory reactions in the CNS and regulated the LPS-induced TNF-a biosynthesis in rat astrocytes. Moreover, SSeCKS was involved in LPS-induced PKC-ERK signaling pathways in LPS-treated rat astrocytes (Sun et al 2007b;Yan et al 2007a). In current study, we also showed that LPS induced astrocytes activation and up-regulated the expression of SSeCKS in astrocytes.…”

Section: Discussionsupporting

confidence: 60%

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

Shao

Yang

et al. 2011

Cell Mol Neurobiol

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Src-suppressed C kinase substrate (SSeCKS), a protein kinase C substrate, is a major lipopolysaccharide (LPS) response protein. In addition, β-1,4 Galactosyltransferase-I (β-1,4-GalT-I) also plays an important role in the inflammation reactions of nervous system. It was reported that both SSeCKS and β-1,4-GalT-I were involved in the LPS-induced tumor necrosis factor-alpha (TNF-α) expression in rat primary astrocytes. However, the functional interaction between SSeCKS and β-1,4-GalT-I in the LPS-induced TNF-α 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 β-1,4-GalT-I participated in LPS-induced TNF-α secretion through p38, JNK, and ERK signal transduction pathways in rat primary astrocytes. Knockdown by small-interfering RNAs (siRNAs) or overexpression of SSeCKS and β-1,4-GalT-I could influence Mitogen-activated protein kinases (MAPKs) signaling pathways activation and TNF-α secretion. Besides, we confirmed that knockdown of SSeCKS could prevent the induction of β-1,4-GalT-I in this process. Inversely, β-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-α secretion through β-1,4-GalT-I in rat primary astrocytes.

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Section: Discussionsupporting

confidence: 60%

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

Shao

Yang

et al. 2011

Cell Mol Neurobiol

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“…It also restored normal actin-based cytoskeletal architecture and cell-cycle controls on cyclin D1 expression (Lin and Gelman 1997;Xia et al 2001). Here we provided new evidence showing that TNF-a up-regulated the expression of SSeCKS in SCs in a dose-dependent manner that was similar in astrocytes and C6 glioma cells (Sun et al 2007a;Yan et al 2007). Furthermore, the concentration-dependent increase in SSeCKS mRNA and protein levels were accompanied by a reduced expression of cyclin D1.…”

Section: Discussionmentioning

confidence: 61%

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

Tao

Cheng

et al. 2009

Journal of Neurochemistry

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Src‐suppressed protein kinase C substrate (SSeCKS) is a protein kinase C substrate protein, which plays an important role in mitogenic regulatory activity. In the early stage of nerve injury, expression of SSeCKS in the PNS increases, mainly in Schwann cells (SCs). However, the exact function of SSeCKS in the regulation of SC proliferation remains unclear. In this study, we found that tumor necrosis factor‐alpha (TNF‐α) induced both SSeCKS α isoform expression and SC growth arrest in a dose‐dependent manner. By knocking down SSeCKS α isoform expression, TNF‐α‐induced growth arrest in SCs was partially rescued. Concurrently, the expression of cyclin D1 was reduced and the activity of extracellular signal‐regulated kinase 1/2 was decreased. A luciferase activity assay showed that cyclin D1 expression was regulated by SSeCKS at the transcription level. In addition, the cell fragments assay and immunofluorescence revealed that TNF‐α prevented the translocation of cyclin D1 into the nucleus, while knocking down SSeCKS α isoform expression prompted cyclin D1 redistribution to the nucleus. In summary, our data indicate that SSeCKS may play a critical role in TNF‐α‐induced SC growth arrest through inhibition of cyclin D1 expression thus preventing its nuclear translocation.

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“…Cellular iNOS production depends on PKC activity as well as the availability of ERK1/2, which is controlled by enzymes such as MEK in glial cells [37,38]. Our previous data indicated SSeCKS was involved in LPS-induced PKC-ERK Signaling Pathways and played a regulatory role in the TNF-α biosynthesis in LPS-treated rat astrocytes [18,21]. SSeCKS has a motif for binding PKC/PKA, is the substrate of PKC, and is phosphorylated by PKC [37].…”

Section: Discussionmentioning

confidence: 95%

“…Numerous studies have demonstrated that PKC is essential for the induction of proinflammatory cytokine (tumor necrosis factor-alpha (TNF-α), inducible nitric oxide synthase (iNOS)) in astrocytes [19,20]. Our previous data also indicated that SSeCKS played a regulatory role in TNF-α biosynthesis in rat astrocytes after LPS treatment [18,21]. However, the role of SSeCKS in LPS-induced iNOS biosynthesis was not shown yet.…”

Section: Introductionmentioning

confidence: 83%

Involvement of Src-Suppressed C Kinase Substrate in Neuronal Death Caused by the Lipopolysaccharide-Induced Reactive Astrogliosis

et al. 2010

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Src-suppressed C kinase substrate (SSeCKS), a protein kinase C substrate, is a major lipopolysaccharide (LPS) response protein, regulating the inflammatory process. In the process of spinal inflammatory diseases by LPS intraspinal injection, expression of SSeCKS in the spinal cord was increased, mainly in active astrocytes and neurons. Induced SSeCKS was colabeled with terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling (an apoptosis maker) in the late inflammation processes. These results indicated that SSeCKS might correlate with the inflammatory reaction and late neurodegeneration after LPS injection. A cell type-specific action for SSeCKS was further studied within C6 cells and PC12 cells. Knockdown of SSeCKS by small-interfering RNAs (siRNAs) blocked the LPS-induced inducible nitric oxide synthase (iNOS) expression in C6 cells, while overexpression SSeCKS enhanced iNOS expression. SSeCKS is also participated in regulation of PC12 cell viability. Loss of SSeCKS rescued PC12 cell viability, and excessive SSeCKS exacerbated the cell death upon conditioned medium and tumor necrosis factor-alpha exposure. This study delineates that SSeCKS may be important for host defenses in spinal inflammation and suggests a valuable molecular mechanism by which astrocytes modify neuronal viability during pathological states.

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The role of TNF-α and its receptors in the production of Src-suppressed C kinase substrate by rat primary type-2 astrocytes

Cited by 16 publications

References 21 publications

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

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

Tumor necrosis factor‐alpha inhibits Schwann cell proliferation by up‐regulating Src‐suppressed protein kinase C substrate expression

Involvement of Src-Suppressed C Kinase Substrate in Neuronal Death Caused by the Lipopolysaccharide-Induced Reactive Astrogliosis

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