Astrogliosis induced by brain injury is regulated by sema4B phosphorylation

Liat Ben-Gigi, Sahar Sweetat, Elazar Besser, Yakov Fellig, Thorsten Wiederhold, Roberto D. Polakiewicz, Oded Behar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


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.

Original languageAmerican English
Article numbere0078-14.2015
Issue number3
StatePublished - 1 May 2015

Bibliographical note

Publisher Copyright:
© 2015 Ben-Gigi et al.


  • Astrogliosis
  • CNS injury
  • Sema4B


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