A switch in pdgfrb+ cell-derived ECM composition prevents inhibitory scarring 
and promotes axon regeneration in the zebrafish spinal cord

Tsata, Vasiliki; Möllmert, Stephanie; Schweitzer, Christine; Kolb, Julia; Möckel, Conrad; Böhm, Benjamin; Rosso, Gonzalo; Lange, Christian; Lesche, Mathias; Hammer, Juliane; Kesavan, Gokul; Beis, Dimitris; Guck, Jochen; Brand, Michael; Wehner, Daniel

doi:10.1016/j.devcel.2020.12.009

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A switch in pdgfrb+ cell-derived ECM composition prevents inhibitory scarring and promotes axon regeneration in the zebrafish spinal cord

MPS-Authors

/persons/resource/persons255608

Möllmert, Stephanie
Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;

/persons/resource/persons255610

Schweitzer, Christine
Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;

/persons/resource/persons255612

Kolb, Julia
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;
Wehner Research Group, Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;

/persons/resource/persons255614

Möckel, Conrad
Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;

/persons/resource/persons255616

Böhm, Benjamin
Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;

/persons/resource/persons248155

Rosso, Gonzalo
Guests, Max Planck Institute for the Science of Light, Max Planck Society;
Institute of Physiology II, University of Münster;

/persons/resource/persons241284

Guck, Jochen
Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;
Biotechnology Center, Center for Molecular and Cellular Bioengineering, Technische Universität Dresden;

/persons/resource/persons255618

Wehner, Daniel
Max-Planck-Zentrum für Physik und Medizin, Max Planck Institute for the Science of Light, Max Planck Society;
Wehner Research Group, Guck Division, Max Planck Institute for the Science of Light, Max Planck Society;

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引用

Tsata, V., Möllmert, S., Schweitzer, C., Kolb, J., Möckel, C., Böhm, B., Rosso, G., Lange, C., Lesche, M., Hammer, J., Kesavan, G., Beis, D., Guck, J., Brand, M., & Wehner, D. (2021). A switch in pdgfrb+ cell-derived ECM composition prevents inhibitory scarring and promotes axon regeneration in the zebrafish spinal cord. Developmental Cell, 56(4), 509-524. doi:10.1016/j.devcel.2020.12.009.

引用: https://hdl.handle.net/21.11116/0000-0007-A7F8-5

要旨

In mammals, perivascular cell-derived scarring after spinal cord injury impedes axonal regrowth. In contrast, the extracellular matrix (ECM) in the spinal lesion site of zebrafish is permissive and required for axon regeneration. However, the cellular mechanisms underlying this interspecies difference have not been investigated. Here, we show that an injury to the zebrafish spinal cord triggers recruitment of pdgfrb+ myoseptal and perivascular cells in a PDGFR signaling-dependent manner. Interference with pdgfrb+ cell recruitment or depletion of pdgfrb+ cells inhibits axonal regrowth and recovery of locomotor function. Transcriptional profiling and functional experiments reveal that pdgfrb+ cells upregulate expression of axon growth-promoting ECM genes (cthrc1a and col12a1a/b) and concomitantly reduce synthesis of matrix molecules that are detrimental to regeneration (lum and mfap2). Our data demonstrate that a switch in ECM composition is critical for axon regeneration after spinal cord injury and identify the cellular source and components of the growth-promoting lesion ECM.