NDLI: The Role of TNF-α and its Receptors in the Production of β-1,4-galactosyltransferase I mRNA by Rat Primary Type-2 Astrocytes

Content Provider	Springer Nature Link
Author	Yan, Meijuan Xia, Chunlin Niu, Shuqiong Cheng, Chun Shao, Xiaoyi Shen, Aiguo
Copyright Year	2007
Abstract	β-1,4-galactosyltransferase I (β-1,4-GalT I) plays an important role in the synthesis of the backbone structure of adhesion molecules involved in leukocyte–endothelial cell interaction. The expression of β-1,4-GalT I mRNA increased in primary human endothelial cells after exposure to tumor necrosis factor-α (TNF-α). In the central nervous system (CNS), astrocytes play a pivotal role in immunity as immunocompetent cells by secreting cytokines and inflammatory mediators, there are two types of astrocytes. Type-1 astrocytes can secrete TNF-α when stimulated with Lipopolysaccharide (LPS), while the responses of type-2 astrocytes during inflammation are unknown. So we examined the expression change of β-1,4-GalT I mRNA in type-2 astrocytes after exposure to TNF-α and LPS. Real-time PCR showed that TNF-α or LPS affected β-1,4-GalT I mRNA expression in a time- and dose-dependent manner. RT-PCR analysis revealed that TNFR1 and TNFR2 were present in normal untreated type-2 astrocytes, and that TNF-α, TNFR1 and TNFR2 increased in type-2 astrocytes after exposure to TNF-α or LPS. Immunocytochemistry showed that TNFR1 was expressed in the cytoplasm, nucleus and processes of normal untreated type-2 astrocytes, and distributed mainly in the cytoplasm and processes after exposure to LPS. TNFR2 was mainly expressed in the nucleus of normal untreated type-2 astrocytes, and distributed mainly in the processes of type-2 astrocytes after exposure to LPS. Both anti-TNFR1 and anti-TNFR2 antibodies suppressed β-1,4-GalT I mRNA expression induced by TNF-α or LPS. From these results, we conclude that TNF-α signaling via both TNFR1 and TNFR2 translocated from nucleus to cytoplasm or processes is sufficient to induce β-1,4-GalT I mRNA. In addition, we observed that not only exogenous TNF-α but also TNF-α produced by type-2 astrocytes affected β-1,4-GalT I mRNA production in type-2 astrocytes. These results suggest that an autocrine loop involving TNF-α contributes to the production of β-1,4-GalT I mRNA in response to inflammation.
Starting Page	223
Ending Page	236
Page Count	14
File Format	PDF
ISSN	02724340
Journal	Cellular and Molecular Neurobiology
Volume Number	28
Issue Number	2
e-ISSN	15736830
Language	English
Publisher	Springer US
Publisher Date	2007-08-22
Publisher Place	Boston
Access Restriction	Subscribed
Subject Keyword	Tumor necrosis factor-α Tumor necrosis factor receptors Lipopolysaccharide β-1,4-galactosyltransferase I Type-2 astrocyte Rat Animal Anatomy / Morphology / Histology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Cellular and Molecular Neuroscience

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