Up-regulation of Dyrk1b promote astrocyte activation following lipopolysaccharide-induced neuroinflammation.

Astrocytes become activated in response to different stimulation. Dyrk1b is an arginine-directed serine/threonineprotein kinase that is expressed at elevated levels in many cancers but remains unknown in the pathologies of neuroinflammation. In this study, in vivo, we demonstrated that Dyrk1b expression was significantly increased and reached a peak at 12 h after LPS injection via Western blot. Double immunofluorescence staining showed that Dyrk1b co-located with GFAP and Ki67. In vitro, the expression of Dyrk1b, Ki67 and cyclinD1 was gradually increased and reached a peak at 12 h in a time-dependent manner after 1 μg/mL LPS stimulation. Knockdown of Dyrk1b significantly reduced the expression of Ki67 and cyclinD1. In addition, the data exhibited that silenced Dyrk1b decreased the expression of p-STAT3 in primary astrocyte cells, and Dyrk1b interacted with STAT3 in LPS-induced neuroinflammation. In conclusion, these results suggested that Dyrk1b is increased and may play a crucial role in regulating astrocyte cell activation via interact with STAT3 in LPS-induced neuroinflammation.