Astrogliosis Induced by Brain Injury Is Regulated by Sema4B Phosphorylation123
| Autor: | Ben-Gigi, Liat, Sweetat, Sahar, Besser, Elazar, Fellig, Yakov, Wiederhold, Thorsten, Polakiewicz, Roberto D., Behar, Oded |
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| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: | |
| Zdroj: | eNeuro |
| ISSN: | 2373-2822 |
| Popis: | Astrocyte activation plays a critical role in response to CNS trauma. Following CNS injury, astrogliosis has the beneficial effect of restricting tissue damage, but it also limits neuronal regeneration. 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. |
| Databáze: | OpenAIRE |
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