Key result
Periostin expression is stimulated by the ErbB ligand NRG1 and significantly influences the migration of Schwann cell precursors in mouse models.
Periostin, stimulated by NRG1, plays a crucial role in the migration of Schwann cell precursors in the peripheral nervous system.
Caution against clinical use in nerve repair; leaves open therapeutic targeting of NRG1-Periostin in humans.
Neuregulin ligands and their ErbB receptors are important for the development of Schwann cells, the glial cells of the peripheral nervous system (PNS). ErbB3 deficiency is characterized by a complete loss of Schwann cells along axons of the peripheral nerves, impaired fasciculation and neuronal cell death. We performed comparative gene expression analysis of dorsal root ganglia (DRG) explant cultures from ErbB3-deficient and wild-type mice in order to identify genes that are involved in Schwann cell development and migration. The extracellular matrix (ECM) gene periostin was found to exhibit the most prominent down regulation in ErbB3-deficient DRG. Expression analysis revealed that the periostin-expressing cell population in the PNS corresponds to Schwann cell precursors and Schwann cells, and is particularly high in migratory Schwann cells. Furthermore, stimulation of Schwann cells with neuregulin-1 (NRG1) or transforming growth factor β (TGFβ-1) resulted in an upregulation of periostin expression. Interestingly, DRG explant cultures of periostin-deficient mice revealed a significant reduction of the number of migrating Schwann cells. These data demonstrate that the expression of periostin is stimulated by ErbB ligand NRG1 and influences the migration of Schwann cell precursors.
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Sonnenberg-Riethmacher et al. (2015) studied Schwann cell development and migration. ErbB3 deficiency, periostin deficiency, and NRG1/TGFβ-1 stimulation vs. Wild-type mice and unstimulated cells was evaluated on Periostin expression levels and number of migrating Schwann cells. Periostin expression is stimulated by the ErbB ligand NRG1 and significantly influences the migration of Schwann cell precursors in mouse models.
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