Neurobiology in the Geller Lab  
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Structure/Function Relationships of Glycosaminoglycan Chains

GAG Chain Receptors

Intracellular Signaling Pathways

Astrocyte Extracellular Matrix

Biophysics of Growth Cones

Tissue Engineering

Lab Protocols

Laboratory of Developmental Neurobiology
Division of Intramural Research, NHLBI
Bethesda, MD 20892-1754

Geller Lab Research > Astrocyte Extracellular Matrix

Astrocytes are the major cell type of the brain, whose numbers far surpass that of neurons.  In the uninjured brain, astrocytes surround neurons and provide nourishment. After injury, astrocytes become hypertrophic and change their physiology to become a major part of the glial scar that inhibits regeneration.  This inhibition is primarily mediated by an increased secretion of extracellular matrix ECM) molecules, especially chondroitin sulfate proteoglycans.  Our research is focused on understanding the regulatory mechanisms that result in this secretion and in changing the composition of the ECM, as well as identifying methods to reduce it and promote regeneration and recovery of function. 

• Pearson, C. S., Solano, A. G., Tilve, S., Mencio, C. P., Martin, K. R. and Geller, H. M. Spatiotemporal distribution of chondroitin sulfate proteoglycans after optic nerve injury in rodents, Exptl. Eye Res., in press.

• Jin, J., Tilve, S., Huang, Z., Geller, H. M., Yu, P. The effect of CSPGs on neuronal cell adhesion, spreading and neurite growth in culture, Neural Regen. Res., 13:289-297, 2018.

• George, N. and Geller, H. M. Extracellular matrix and traumatic brain injury, J. Neurosci. Res., 96:573-588, 2018.

 • Yi, M., Wei, T., Wang, Y., Liu, Q.,  Yu, P., Lu, Q., Chen, G., Gao, X., Geller, H. M., Chen, H. and Yu, Z.  The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke,  J. Neuroinflamm., 14:203, 2017

• Yi, M., Yu, P., Lu, Q., Geller, H. M. Yu, Z., and Chen, H. KCa3.1 constitutes a pharmacological target for astrogliosis associated with Alzheimer's Disease, Mol. Cell. Neurosci., S1044-7431, 2016

• Susarla, B., Villapol, S., Yi, J. H., Geller, H. M., Symes, A. J. Temporal patterns of cortical proliferation of glial cell populations after traumatic brain injury in mice, ASN Neuro, 6:159-70 2014.

• Yu, Z.-H., Yu, P., Chen, H.-Z., Geller, H. M. Targeted inhibition of KCa3.1 attenuates TGF-β-induced reactive astrogliosis through the Smad2/3 signaling pathway, J. Neurochem., 130:41-9, 2014

• Yi, J. H., Katagiri, Y., Susarla, B., Figge, D., Symes, A. J. and Geller, H. M. Detection of sulfated chondroitin glycosaminoglycans following controlled cortical impact injury in mice, J. Comp. Neurol., 520:3295-313, 2012.

• Yu, P., Wang, H., Katagiri, Y. and Geller, H. M. An in vitro model of reactive astrogliosis and its effect on neuronal growth. In: Astrocytes, Methods and Protocols, R. Milner, ed., Humana Press, Methods in Molecular Biology, 814:327-40, 2012

• Susarla, B. T. S., Laing, E. D., Yu, P., Katagiri, Y., Geller, H. M. and Symes, A. J. SMAD proteins differentially regulate TGF-β mediated induction of chondroitin sulfate proteoglycans, J. Neurochem., 119:868-78, 2011.

• Laabs, T., Wang, H., McCann, T. E., Katagiri, Y., Fawcett, J. W . and Geller, H. M. Inhibiting GAG chain polymerization decreases the inhibitory activity of astrocyte-derived chondroitin sulfate proteoglycans, J. Neurosci., 27:14494-14501, 2007.

• Powell, E. M., Calle-Patino, Y. A., Mercado, M. L. T. and Geller, H. M. Protein kinase C mediates neurite guidance at an astrocyte boundary, Glia, 33:288-297, 2001.