Multiple sclerosis (MS) is a progressive neuro-inflammatory disorder, characterized by immune cell influx, demyelination, and by axonal dysfunction and neurodegeneration. To date, the underlying mechanisms of impaired neuronal function in MS are not fully understood, but evidence is accumulating that activated glial cells may play a role in this detrimental process. In MS, reactive astrocytes form a gliotic scar, marked by excessive production of extracellular matrix molecules, which is postulated to impair neuronal function. In the current study, researchers of the MS center Amsterdam show that the astrocytic cation channel Transient Receptor Potential, subfamily M, member 7 (TRPM7) is a novel player in the formation of a gliotic scar. TRPM7 is highly expressed in reactive astrocytes within well-characterized human MS lesions and its expression is induced in primary astrocytes under chronic inflammatory conditions. In addition, astrocytes that express high levels of TRPM7 impair neuronal outgrowth through the production of chondroitin sulfate proteoglycans, a key component of the gliotic scar. These findings indicate that astrocytic TRPM7 is a critical regulator of the formation of a gliotic scar and provide a novel mechanism by which reactive astrocytes affect neuronal outgrowth.
Read more: https://www.ncbi.nlm.nih.gov/pubmed/30453391.
Kamermans A, Planting KE, Jalink K, van Horssen J, de Vries HE. Reactive astrocytes in multiple sclerosis impair neuronal outgrowth through TRPM7-mediated chondroitin sulfate proteoglycan production. Glia. 2018 Nov 19. doi: 10.1002/glia.23526.