Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Apr 30;5(2):021505.
doi: 10.1063/5.0037814. eCollection 2021 Jun.

Mechanotransduction assays for neural regeneration strategies: A focus on glial cells

Affiliations
Review

Mechanotransduction assays for neural regeneration strategies: A focus on glial cells

Nicolas Marinval et al. APL Bioeng. .

Abstract

Glial cells are mechanosensitive, and thus, engineered systems have taken a step forward to design mechanotransduction platforms in order to impart diverse mechanical stresses to cells. Mechanical strain encountered in the central nervous system can arise from diverse mechanisms, such as tissue reorganization, fluid flow, and axon growth, as well as pathological events including axon swelling or mechanical trauma. Biomechanical relevance of the in vitro mechanical testing requires to be placed in line with the physiological and mechanical changes in central nervous tissues that occur during the progression of neurodegenerative diseases. Mechanotransduction signaling utilized by glial cells and the recent approaches intended to model altered microenvironment adapted to pathological context are discussed in this review. New insights in systems merging substrate's stiffness and topography should be considered for further glial mechanotransduction studies, while testing platforms for drug discoveries promise great advancements in pharmacotherapy. Potential leads and strategies for clinical outcomes are expected to be developed following the exploration of these glial mechanosensitive signaling pathways.

PubMed Disclaimer

Figures

FIG 1.
FIG 1.
Glial mechanotransduction pathways and pharmacological inhibitors.
FIG. 2.
FIG. 2.
Glial mechanotransduction platforms and assays.

References

    1. Kim S. Y., Porter B. E., Friedman A., and Kaufer D., “ A potential role for glia-derived extracellular matrix remodeling in postinjury epilepsy,” J. Neurosci. Res. 94, 794–803 (2016).10.1002/jnr.23758 - DOI - PubMed
    1. Song I. and Dityatev A., “ Crosstalk between glia, extracellular matrix and neurons,” Brain Res. Bull. 136, 101–108 (2018).10.1016/j.brainresbull.2017.03.003 - DOI - PubMed
    1. Barnes J. M., Przybyla L., and Weaver V. M., “ Tissue mechanics regulate brain development, homeostasis and disease,” J. Cell Sci. 130, 71–82 (2017).10.1242/jcs.191742 - DOI - PMC - PubMed
    1. Humphrey J. D., Dufresne E. R., and Schwartz M. A., “ Mechanotransduction and extracellular matrix homeostasis,” Nat. Rev. Mol. Cell Biol. 15, 802–812 (2014).10.1038/nrm3896 - DOI - PMC - PubMed
    1. Hemphill M. A., Dauth S., Yu C. J., Dabiri B. E., and Parker K. K., “ Traumatic brain injury and the neuronal microenvironment: A potential role for neuropathological mechanotransduction,” Neuron 85, 1177–1192 (2015).10.1016/j.neuron.2015.02.041 - DOI - PubMed

LinkOut - more resources