RT Journal Article
SR Electronic
T1 Astrogliosis Induced by Brain Injury Is Regulated by Sema4B Phosphorylation
JF eneuro
JO eneuro
FD Society for Neuroscience
SP ENEURO.0078-14.2015
DO 10.1523/ENEURO.0078-14.2015
VO 2
IS 3
A1 Ben-Gigi, Liat
A1 Sweetat, Sahar
A1 Besser, Elazar
A1 Fellig, Yakov
A1 Wiederhold, Thorsten
A1 Polakiewicz, Roberto D.
A1 Behar, Oded
YR 2015
UL http://www.eneuro.org/content/2/3/ENEURO.0078-14.2015.abstract
AB Injury to the CNS induces astrogliosis, an astrocyte-mediated response that has both beneficial and detrimental impacts on surrounding neural and non-neural cells. The precise signaling events underlying astrogliosis are not fully characterized. Here, we show that astrocyte activation was altered and proliferation was reduced in Semaphorin 4B (Sema4B)-deficient mice following injury. Proliferation of cultured Sema4B−/− astrocytes was also significantly reduced. In contrast to its expected role as a ligand, the Sema4B ectodomain was not able to rescue Sema4B−/− astrocyte proliferation but instead acted as an antagonist against Sema4B+/− astrocytes. Furthermore, the effects of Sema4B on astrocyte proliferation were dependent on phosphorylation of the intracellular domain at Ser825. Our results suggest that Sema4B functions as an astrocyte receptor, defining a novel signaling pathway that regulates astrogliosis after CNS injury.