Chondroitin sulfate proteoglycans as mediators of axon growth and pathfinding

1997 ◽  
Vol 290 (2) ◽  
pp. 343-348 ◽  
Author(s):  
Richard U. Margolis ◽  
Renée K. Margolis
Keyword(s):  
Chondroitin Sulfate ◽  
Axon Growth ◽  
Chondroitin Sulfate Proteoglycans

scholarly journals Integrin Activation Promotes Axon Growth on Inhibitory Chondroitin Sulfate Proteoglycans by Enhancing Integrin Signaling

2011 ◽  
Vol 31 (17) ◽  
pp. 6289-6295 ◽  
Author(s):  
C. L. Tan ◽  
J. C. F. Kwok ◽  
R. Patani ◽  
C. ffrench-Constant ◽  
S. Chandran ◽  
...  
Keyword(s):  
Chondroitin Sulfate ◽  
Axon Growth ◽  
Chondroitin Sulfate Proteoglycans ◽  
Integrin Signaling ◽  
Integrin Activation

scholarly journals Kindlin-1 Enhances Axon Growth on Inhibitory Chondroitin Sulfate Proteoglycans and Promotes Sensory Axon Regeneration

2012 ◽  
Vol 32 (21) ◽  
pp. 7325-7335 ◽  
Author(s):  
C. L. Tan ◽  
M. R. Andrews ◽  
J. C. F. Kwok ◽  
T. G. P. Heintz ◽  
L. F. Gumy ◽  
...  
Keyword(s):  
Chondroitin Sulfate ◽  
Axon Regeneration ◽  
Axon Growth ◽  
Chondroitin Sulfate Proteoglycans ◽  
Sensory Axon

scholarly journals Semaphorin 3A Binds to the Perineuronal Nets via Chondroitin Sulfate Type E Motifs in Rodent Brains

2013 ◽  
Vol 288 (38) ◽  
pp. 27384-27395 ◽  
Author(s):  
Gunnar Dick ◽  
Chin Lik Tan ◽  
Joao Nuno Alves ◽  
Erich M. E. Ehlert ◽  
Gregory M. Miller ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Chondroitin Sulfate ◽  
Rat Brain ◽  
Core Protein ◽  
Axon Growth ◽  
Chondroitin Sulfate Proteoglycans ◽  
Perineuronal Nets ◽  
Chondroitinase Abc ◽  
Blocking Antibody ◽  
Guidance Molecule

Chondroitin sulfate (CS) and the CS-rich extracellular matrix structures called perineuronal nets (PNNs) restrict plasticity and regeneration in the CNS. Plasticity is enhanced by chondroitinase ABC treatment that removes CS from its core protein in the chondroitin sulfate proteoglycans or by preventing the formation of PNNs, suggesting that chondroitin sulfate proteoglycans in the PNNs control plasticity. Recently, we have shown that semaphorin3A (Sema3A), a repulsive axon guidance molecule, localizes to the PNNs and is removed by chondroitinase ABC treatment (Vo, T., Carulli, D., Ehlert, E. M., Kwok, J. C., Dick, G., Mecollari, V., Moloney, E. B., Neufeld, G., de Winter, F., Fawcett, J. W., and Verhaagen, J. (2013) Mol. Cell. Neurosci. 56C, 186–200). Sema3A is therefore a candidate for a PNN effector in controlling plasticity. Here, we characterize the interaction of Sema3A with CS of the PNNs. Recombinant Sema3A interacts with CS type E (CS-E), and this interaction is involved in the binding of Sema3A to rat brain-derived PNN glycosaminoglycans, as demonstrated by the use of CS-E blocking antibody GD3G7. In addition, we investigate the release of endogenous Sema3A from rat brain by biochemical and enzymatic extractions. Our results confirm the interaction of Sema3A with CS-E containing glycosaminoglycans in the dense extracellular matrix of rat brain. We also demonstrate that the combination of Sema3A and PNN GAGs is a potent inhibitor of axon growth, and this inhibition is reduced by the CS-E blocking antibody. In conclusion, Sema3A binding to CS-E in the PNNs may be a mechanism whereby PNNs restrict growth and plasticity and may represent a possible point of intervention to facilitate neuronal plasticity.

scholarly journals Deacetylation of Miro1 by HDAC6 blocks mitochondrial transport and mediates axon growth inhibition

2019 ◽  
Vol 218 (6) ◽  
pp. 1871-1890 ◽  
Author(s):  
Ashley L. Kalinski ◽  
Amar N. Kar ◽  
John Craver ◽  
Andrew P. Tosolini ◽  
James N. Sleigh ◽  
...  
Keyword(s):  
Growth Inhibition ◽  
Chondroitin Sulfate ◽  
Histone Deacetylase ◽  
Growth Failure ◽  
Axon Growth ◽  
Chondroitin Sulfate Proteoglycans ◽  
Histone Deacetylase 6 ◽  
Axon Transport ◽  
Mitochondrial Transport ◽  
Myelin Associated Glycoprotein

Inhibition of histone deacetylase 6 (HDAC6) was shown to support axon growth on the nonpermissive substrates myelin-associated glycoprotein (MAG) and chondroitin sulfate proteoglycans (CSPGs). Though HDAC6 deacetylates α-tubulin, we find that another HDAC6 substrate contributes to this axon growth failure. HDAC6 is known to impact transport of mitochondria, and we show that mitochondria accumulate in distal axons after HDAC6 inhibition. Miro and Milton proteins link mitochondria to motor proteins for axon transport. Exposing neurons to MAG and CSPGs decreases acetylation of Miro1 on Lysine 105 (K105) and decreases axonal mitochondrial transport. HDAC6 inhibition increases acetylated Miro1 in axons, and acetyl-mimetic Miro1 K105Q prevents CSPG-dependent decreases in mitochondrial transport and axon growth. MAG- and CSPG-dependent deacetylation of Miro1 requires RhoA/ROCK activation and downstream intracellular Ca2+ increase, and Miro1 K105Q prevents the decrease in axonal mitochondria seen with activated RhoA and elevated Ca2+. These data point to HDAC6-dependent deacetylation of Miro1 as a mediator of axon growth inhibition through decreased mitochondrial transport.

Differences in Host Serotonin Innervation of Intrastriatal Grafts Are Not Determined by a Glial Scar or Chondroitin Sulfate Proteoglycans

2002 ◽  
Vol 177 (1) ◽  
pp. 61-74 ◽  
Author(s):  
Audrey Petit ◽  
Nancy Quenneville ◽  
Annie Vallée ◽  
Philippe Pierret ◽  
Guy Doucet
Keyword(s):  
Chondroitin Sulfate ◽  
Glial Scar ◽  
Chondroitin Sulfate Proteoglycans

NG2, a member of chondroitin sulfate proteoglycans family mediates the inflammatory response of activated microglia

Neuroscience ◽  
2010 ◽  
Vol 165 (2) ◽  
pp. 386-394 ◽  
Author(s):  
Q. Gao ◽  
J. Lu ◽  
Y. Huo ◽  
N. Baby ◽  
E.A. Ling ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Chondroitin Sulfate ◽  
Chondroitin Sulfate Proteoglycans ◽  
Activated Microglia
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