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The soft mechanical signature of glial scars in the central nervous system

Author

Listed:
  • Emad Moeendarbary

    (Development and Neuroscience, University of Cambridge
    Massachusetts Institute of Technology
    University College London)

  • Isabell P. Weber

    (Development and Neuroscience, University of Cambridge)

  • Graham K. Sheridan

    (Development and Neuroscience, University of Cambridge
    School of Pharmacy and Biomolecular Sciences, University of Brighton)

  • David E. Koser

    (Development and Neuroscience, University of Cambridge
    Present address: Department of Clinical Neurobiology, Heidelberg University and German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany)

  • Sara Soleman

    (John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way)

  • Barbara Haenzi

    (John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way)

  • Elizabeth J. Bradbury

    (Wolfson Centre for Age-Related Diseases, King's College London)

  • James Fawcett

    (John van Geest Centre for Brain Repair, University of Cambridge, Robinson Way)

  • Kristian Franze

    (Development and Neuroscience, University of Cambridge)

Abstract

Injury to the central nervous system (CNS) alters the molecular and cellular composition of neural tissue and leads to glial scarring, which inhibits the regrowth of damaged axons. Mammalian glial scars supposedly form a chemical and mechanical barrier to neuronal regeneration. While tremendous effort has been devoted to identifying molecular characteristics of the scar, very little is known about its mechanical properties. Here we characterize spatiotemporal changes of the elastic stiffness of the injured rat neocortex and spinal cord at 1.5 and three weeks post-injury using atomic force microscopy. In contrast to scars in other mammalian tissues, CNS tissue significantly softens after injury. Expression levels of glial intermediate filaments (GFAP, vimentin) and extracellular matrix components (laminin, collagen IV) correlate with tissue softening. As tissue stiffness is a regulator of neuronal growth, our results may help to understand why mammalian neurons do not regenerate after injury.

Suggested Citation

  • Emad Moeendarbary & Isabell P. Weber & Graham K. Sheridan & David E. Koser & Sara Soleman & Barbara Haenzi & Elizabeth J. Bradbury & James Fawcett & Kristian Franze, 2017. "The soft mechanical signature of glial scars in the central nervous system," Nature Communications, Nature, vol. 8(1), pages 1-11, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14787
    DOI: 10.1038/ncomms14787
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    Cited by:

    1. Xu Feng & Guo-Yang Li & Seok-Hyun Yun, 2023. "Ultra-wideband optical coherence elastography from acoustic to ultrasonic frequencies," Nature Communications, Nature, vol. 14(1), pages 1-13, December.
    2. Julia Kolb & Vasiliki Tsata & Nora John & Kyoohyun Kim & Conrad Möckel & Gonzalo Rosso & Veronika Kurbel & Asha Parmar & Gargi Sharma & Kristina Karandasheva & Shada Abuhattum & Olga Lyraki & Timon Be, 2023. "Small leucine-rich proteoglycans inhibit CNS regeneration by modifying the structural and mechanical properties of the lesion environment," Nature Communications, Nature, vol. 14(1), pages 1-23, December.

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