Abstract

Traumatic injury of peripheral nerves typically also damages nerve surrounding tissue including muscles. Hence, molecular and cellular interactions of neighboring damaged tissues might be decisive for successful axonal regeneration of injured nerves. So far, the contribution of muscles and muscle-derived molecules to peripheral nerve regeneration has only poorly been studied. Herein, we conditionally ablated SRF (serum response factor), an important myofiber transcription factor, in skeletal muscles of mice. Subsequently, the impact of this myofiber-restricted SRF deletion on peripheral nerve regeneration, i.e. facial nerve injury was analyzed. Quantification of facial nerve regeneration by retrograde tracer transport, inspection of neuromuscular junctions (NMJs) and recovery of whisker movement revealed reduced axonal regeneration upon muscle specific Srf deletion. In contrast, responses in brainstem facial motor neuron cell bodies such as regeneration-associated gene (RAG) induction of Atf3, synaptic stripping and neuroinflammation were not overly affected by SRF deficiency. Mechanistically, SRF in myofibers appears to stimulate nerve regeneration through regulation of muscular satellite cell (SC) proliferation. In summary, our data suggest a role of muscle cells and SRF expression within muscles for regeneration of injured peripheral nerves.

Highlights

  • Traumatic injury of peripheral nerves typically damages nerve surrounding tissue including muscles

  • We uncovered that interference with myofiber function by abrogation of the myofiber transcription factor serum response factor (SRF) reduced peripheral nerve regeneration

  • Since the facial nerve analyzed in this study directly navigates along several facial muscles this suggests a paracrine effect of myofibers on injured and re-growing axons

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Summary

Introduction

Traumatic injury of peripheral nerves typically damages nerve surrounding tissue including muscles. Further SRF target genes relevant to muscle function are genes encoding actin isoforms (skeletal actin, Acta[1]; α-cardiac actin, Actc[1]; β-actin, Actb; γ-actin, Actg and smooth muscle actin, Acta2) or actin binding proteins such as calponin and filamins[9,18] It has not been analyzed whether SRF in muscles stimulates peripheral nerve regeneration. In this study we analyzed whether interference with muscle function by SRF depletion modulates the outcome of peripheral nerve regeneration For this we employed myofiber restricted SRF ablation where Cre recombinase expression is driven by the myofiber specific human skeletal actin (HSA) promotor (Srfloxp/loxp: HSA-CreERT2 mice). Muscle restricted SRF depletion interfered with injury induced SC proliferation

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