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Review
. 2024 May;102(5):e25356.
doi: 10.1002/jnr.25356.

Heterogeneity of brain extracellular matrix and astrocyte activation

Rebecca E Huber  1 , Courtney Babbitt  2 , Shelly R Peyton  1
Affiliations
Review

Heterogeneity of brain extracellular matrix and astrocyte activation

Rebecca E Huber et al. J Neurosci Res. 2024 May.

Abstract

From the blood brain barrier to the synaptic space, astrocytes provide structural, metabolic, ionic, and extracellular matrix (ECM) support across the brain. Astrocytes include a vast array of subtypes, their phenotypes and functions varying both regionally and temporally. Astrocytes' metabolic and regulatory functions poise them to be quick and sensitive responders to injury and disease in the brain as revealed by single cell sequencing. Far less is known about the influence of the local healthy and aging microenvironments on these astrocyte activation states. In this forward-looking review, we describe the known relationship between astrocytes and their local microenvironment, the remodeling of the microenvironment during disease and injury, and postulate how they may drive astrocyte activation. We suggest technology development to better understand the dynamic diversity of astrocyte activation states, and how basal and activation states depend on the ECM microenvironment. A deeper understanding of astrocyte response to stimuli in ECM-specific contexts (brain region, age, and sex of individual), paves the way to revolutionize how the field considers astrocyte-ECM interactions in brain injury and disease and opens routes to return astrocytes to a healthy quiescent state.

Keywords: central nervous system; glia; hyaluronan; integrin; lectican; matrix metalloproteinase; multiple sclerosis; tenascin.

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References

REFERENCES

    1. Adams, J. C., & Tucker, R. P. (2000). The thrombospondin type 1 repeat (TSR) superfamily: Diverse proteins with related roles in neuronal development. Developmental Dynamics, 218, 280–299.
    1. Angelov, D. N., Walther, M., Streppel, M., Guntinas‐Lichius, O., Neiss, W. F., Probstmeier, R., & Pesheva, P. (1998). Tenascin‐R is antiadhesive for activated microglia that induce downregulation of the protein after peripheral nerve injury: A new role in neuronal protection. Journal of Neuroscience, 18, 6218–6229.
    1. Avalos, A. M., Valdivia, A. D., Muñoz, N., Herrera‐Molina, R., Tapia, J. C., Lavandero, S., Chiong, M., Burridge, K., Schneider, P., Quest, A. F., & Leyton, L. (2009). Neuronal Thy‐1 induces astrocyte adhesion by engaging syndecan‐4 in a cooperative interaction with alphavbeta3 integrin that activates PKCalpha and RhoA. Journal of Cell Science, 122, 3462–3471.
    1. Back, S. A., Tuohy, T. M. F., Chen, H., Wallingford, N., Craig, A., Struve, J., Luo, N. L., Banine, F., Liu, Y., Chang, A., Trapp, B. D., Bebo, B. F., Jr., Rao, M. S., & Sherman, L. S. (2005). Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation. Nature Medicine, 11, 966–972.
    1. Baron, W., Bijlard, M., Nomden, A., de Jonge, J. C., Teunissen, C. E., & Hoekstra, D. (2014). Sulfatide‐mediated control of extracellular matrix‐dependent oligodendrocyte maturation. Glia, 62, 927–942.

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