The Functional Interaction Between CDK11p58 and β-1,4-Galactosyltransferase I Involved in Astrocyte Activation Caused by Lipopolysaccharide

Glial cells are mediating the main activation of the central nervous system (CNS), being astrocytes the mayor glial cells in the brain. Glial activation may result beneficial since it could promote tissue repair and pathogen elimination. However, excessive glial activation mechanism can also have do harm to the tissue. β-1,4-Galactosyltransferase I (β-1,4-GalT-I) is a key inflammatory mediator that participates in the initiation and maintenance of inflammatory reaction in some diseases. Moreover, CDK11^p58 has been reported to be associated with β-1,4-GalT-I. We have found that CDK11^p58 and β-1,4-GalT-I are induced in lipopolysaccharide (LPS)-challenged rat primary astrocytes in a affinis dose- and time-dependent manner. CDK11^p58 regulates the expression of β-1,4-GalT-I by interacting with it. After the knockdown of CDK11^p58 expression, the expression of β-1,4-GalT-I decreases, and astrocyte activation downregulates. Inversely, the expression of β-1,4-GalT-I increases, and astrocyte activation enhances due to the overexpression of CDK11^p58. Knockdown of β-1,4-GalT-I reduces the activation potentiation caused by the overexpression of CDK11^p58, illustrating the function of CDK11^p58 to promote astrocyte activation depends on β-1,4-GalT-I. The interaction between CDK11^p58 and β-1,4-GalT-I to upregulate astrocyte activation is related to activating p38 and JNK pathways. These findings indicated that the functional interaction between CDK11^p58 and β-1,4-GalT-I may play an important role during astrocyte activation after LPS administration.