RGC-32 facilitates reactive astrocytosis by modulating the expression of axonal guidance molecules

Abstract Response Gene to Complement (RGC)-32 modulates TGF-β-induced extracellular matrix secretion and the ability of astrocytes undergo reactive changes in vivo during experimental autoimmune encephalomyelitis (EAE). However, molecular pathways underlying these effects are still not well understood. In this study, we investigated how lack RGC-32 affects transcriptomic profile expression axonal guidance molecules (AGM) EAE. We performed next-generation RNA sequencing on brain neonatal isolated from wild type (WT) knock-out (KO) mice, either unstimulated or stimulated with TGF-β. Results were then validated by using Real-Time PCR. Spinal cords WT KO mice EAE (at days 0 14) stained immunohistochemistry for astrocyte marker GFAP, AGM, nuclear factor IA (NFIA), a gliogenic transcriptional regulator AGM. Lack had significant impact programs normally associated development whose re-expression is usually seen astrocytes. Connectivity analysis revealed that genes coding AGM particularly affected. found lower transcript levels ephrin receptor A 7 (Epha7), plexin A1 Slit ligand 2 Moreover, our results showed NFIA EPHA7 expressed number expressing acute when compared mice. These suggest might facilitate astrogliosis through regulating NFIA. Veterans Administration Merit Award I01BX001458 (to HR)