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Role of Extracellular Matrix Molecules in CNS Injury, Aging and Neurodegenerative Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 2469

Special Issue Editor


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Guest Editor
Institute of Experimental Medicine of the Academy of Sciences of the Czech Republic, Prague, Czech Republic
Interests: spinal cord injury; aging; Alzheimer’s disease; neurodegeneration; regeneration and plasticity; extracellular matrix; perineuronal nets; memory and learning

Special Issue Information

Dear Colleagues,

In the central nervous system, the composition of the extracellular matrix (ECM) plays a crucial role in almost every step of cellular interactions, from the regulation of diffusion parameters and neuronal excitability to inhibition/activation of synaptic plasticity and axonal growth. All ECM structures, including perisynaptic, perinodal matrix or perineuronal nets (PNNs), respond to neuronal and glial activity in processes of memory and learning. Specialized structures such as PNNs enwrap mostly parvalbumin positive inhibitory interneurons and serve as a neuroprotective barrier and a way to stabilize already established neuronal circuits. Within the processes of aging, after CNS injury or in the progress of neurodegenerative disease, alternation in composition and structure of the ECM niche is significant. This results in an environment which is inhibitory to axonal growth or shows disbalance in synaptic plasticity. Enzymatic digestion experimental therapies and individual/multiple components knockouts have been shown to increase plasticity and regenerative potential under these circumstances and, in cases of neurodegenerative disorders, to reduce memory and learning deficiencies. The role of individual components of ECM, their alteration or their surface modifications is of long-term interest.

Dr. Jiří Růžička
Guest Editor

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Keywords

  • extracellular matrix
  • perineuronal nets
  • spinal cord injury
  • traumatic brain injury
  • neurodegeneration
  • aging

Published Papers (1 paper)

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Research

26 pages, 8357 KiB  
Article
Macrophages Rapidly Seal off the Punctured Zebrafish Larval Brain through a Vital Honeycomb Network Structure
by Dandan Zou, Jie Qin, Wenlong Hu, Zongfang Wei, Yandong Zhan, Yuepeng He, Congjian Zhao and Li Li
Int. J. Mol. Sci. 2022, 23(18), 10551; https://doi.org/10.3390/ijms231810551 - 11 Sep 2022
Cited by 1 | Viewed by 2074
Abstract
There is accumulating evidence that macrophages play additional important roles in tissue damage besides their typical phagocytosis. Although the aggregation of macrophages on injured sites has long been observed, few researchers have focused on the role of the overall structure of macrophage aggregation. [...] Read more.
There is accumulating evidence that macrophages play additional important roles in tissue damage besides their typical phagocytosis. Although the aggregation of macrophages on injured sites has long been observed, few researchers have focused on the role of the overall structure of macrophage aggregation. In this study, we developed a standardized traumatic brain injury (TBI) model in zebrafish larvae to mimic edema and brain tissue spillage symptoms after severe brain trauma. Using time-lapse imaging, we showed that macrophages/microglia in zebrafish larvae responded rapidly and dominated the surface of injured tissue, forming a meaningful honeycomb network structure through their compact aggregation and connection. Disrupting this structure led to fatal edema-like symptoms with severe loss of brain tissue. Using the RNA-Seq, together with the manipulation of in vitro cell lines, we found that collagen IV was indispensable to the formation of honeycomb network structures. Our study thus revealed a novel perspective regarding macrophages forming a protective compact structure with collagen IV. This honeycomb network structure acted as a physical barrier to prevent tissue loss and maintain brain homeostasis after TBI. This study may provide new evidence of macrophages’ function for the rapid protection of brain tissue after brain injury. Full article
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