Nature communications · 2019
NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies.
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Fledrich Robert, Akkermann Dagmar, Schütza Vlad, Abdelaal Tamer A, Hermes Doris, Schäffner Erik, Soto-Bernardini M Clara, Götze Tilmann, Klink Axel, Kusch Kathrin, Krueger Martin, Kungl Theresa, Frydrychowicz Clara, Möbius Wiebke, Brück Wolfgang, Mueller Wolf C, Bechmann Ingo, Sereda Michael W, Schwab Markus H, Nave Klaus-Armin, Stassart Ruth M
Аннотация
In contrast to acute peripheral nerve injury, the molecular response of Schwann cells in chronic neuropathies remains poorly understood. Onion bulb structures are a pathological hallmark of demyelinating neuropathies, but the nature of these formations is unknown. Here, we show that Schwann cells induce the expression of Neuregulin-1 type I (NRG1-I), a paracrine growth factor, in various chronic demyelinating diseases. Genetic disruption of Schwann cell-derived NRG1 signalling in a mouse model of Charcot-Marie-Tooth Disease 1A (CMT1A), suppresses hypermyelination and the formation of onion bulbs. Transgenic overexpression of NRG1-I in Schwann cells on a wildtype background is sufficient to mediate an interaction between Schwann cells via an ErbB2 receptor-MEK/ERK signaling axis, which causes onion bulb formations and results in a peripheral neuropathy reminiscent of CMT1A. We suggest that diseased Schwann cells mount a regeneration program that is beneficial in acute nerve injury, but that overstimulation of Schwann cells in chronic neuropathies is detrimental.
Предметные рубрики MeSH
AnimalsAnimals, Genetically ModifiedCharcot-Marie-Tooth DiseaseDemyelinating DiseasesDiabetes Mellitus, Type 1Diabetic NeuropathiesHumansMAP Kinase Signaling SystemMiceMice, TransgenicMicroscopy, ElectronMotor ActivityMyelin ProteinsNeuregulin-1Neuritis, Autoimmune, ExperimentalNeurogliaParacrine CommunicationRatsErb-b2 Receptor Tyrosine KinasesSchwann CellsSciatic NerveSignal TransductionSural NerveTibial Nerve