Expression profiling of Rab GTPases reveals the involvement of Rab20 and Rab32 in acute brain inflammation in mice.

Rab GTPases have emerged as central regulators of vesicle trafficking and are essential for cytokine production during the pathogenesis of neuroinflammation. To characterize the roles of different Rab proteins in brain inflammation, we used quantitative PCR (qPCR) to examine the expression profiles of all members of the Rab family in an experimental model of brain inflammation in mice. We found that Rab20 and Rab32 were substantially up-regulated during the acute phase of inflammation. The increased expression of Rab20 was also confirmed by immunostaining of inflamed brains at different timepoints. The concomitant overexpression of Rabs (Rab20 and Rab32) and early response proinflammatory cytokines (TNF-α and IL-1β) suggested that these Rabs may be important for subsequent inflammatory responses in brain. Furthermore, we found that the expression of certain Rabs was dramatically reduced in cultured primary microglia, which was not observed in the in vivo profiling. In N9, a microglial cell line, however, there was no increase in the expression of Rab20 or Rab32, but Rab3c was significantly overexpressed. These results collectively indicate that Rabs may participate in inflammatory response in microglia during brain inflammation. The differential regulation of individual Rabs in different experimental systems is a caveat for the analysis of Rab functions.