Knocking Down Glycosaminoglycan Synthesis

Wong, Jeffrey

doi:10.1523/jneurosci.0079-08.2008

Cited by 2 publications

(4 citation statements)

References 5 publications

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“…Cortical neurons cultured on laminin matrix (4,5,6). Cortical neurons cultured on Laminin + CSPGs matrix (7,8,9). Cortical neurons cultured on Laminin + CSPGs matrix and treated with 15 ng mL −1 PTN (10,11,12).…”

Section: Activating the Akt Pathway Drives Neurite Growthmentioning

confidence: 99%

“…Cortical neurons cultured on Laminin + CSPGs matrix and treated with 15 ng mL −1 PTN with 1.25 nM alectinib (13,14,15). After 72 hours incubation neurons were stained for Hoechst (4,7,10,13) and MAP2 (5,8,11,14) with Alexa fluor 647. Scale bar: 30 µm.…”

Section: Activating the Akt Pathway Drives Neurite Growthmentioning

confidence: 99%

“…Both ChABC and RNAi are exogenous macromolecules that must be delivered directly to the injury site, have short half-lives in vivo, and could induce immunological response due to repeated administration. 8 Potentiating regeneration of neurons without degrading the glial scar may be possible via the heparin-binding growth factor pleiotrophin (PTN). PTN has long half life 9 , 10 and may overcome the disadvantage of repeated administration associated with the use of ChABC and RNAi.…”

Section: Introductionmentioning

confidence: 99%

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Pleiotrophin Signals Through ALK Receptor to Enhance the Growth of Neurons in the Presence of Inhibitory Chondroitin Sulfate Proteoglycans

et al. 2023

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Chondroitin sulfate proteoglycans (CSPGs), one of the major extracellular matrix components of the glial scar that surrounds central nervous system (CNS) injuries, are known to inhibit the regeneration of neurons. This study investigated whether pleiotrophin (PTN), a growth factor upregulated during early CNS development, can overcome the inhibition mediated by CSPGs and promote the neurite outgrowth of neurons in vitro. The data showed that a CSPG matrix inhibited the outgrowth of neurites in primary cortical neuron cultures compared to a control matrix. PTN elicited a dose-dependent increase in the neurite outgrowth even in the presence of the growth inhibitory CSPG matrix, with optimal growth at 15 ng mL−1 of PTN (114.8% of neuronal outgrowth relative to laminin control). The growth-promoting effect of PTN was blocked by inhibition of the receptor anaplastic lymphoma kinase (ALK) by alectinib in a dose-dependent manner. Neurite outgrowth in the presence of this CSPG matrix was induced by activation of the protein kinase B (AKT) pathway, a key downstream mediator of ALK activation. This study identified PTN as a dose-dependent regulator of neurite outgrowth in primary cortical neurons cultured in the presence of a CSPG matrix and identified ALK activation as a key driver of PTN-induced growth.

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Section: Activating the Akt Pathway Drives Neurite Growthmentioning

confidence: 99%

Section: Activating the Akt Pathway Drives Neurite Growthmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Pleiotrophin Signals Through ALK Receptor to Enhance the Growth of Neurons in the Presence of Inhibitory Chondroitin Sulfate Proteoglycans

et al. 2023

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“…Although these strategies have shown positive effects on the growth of neurons in model systems, there are disadvantages that may limit translation to clinical use. Both ChABC and siRNA are exogenous macromolecules that must be delivered directly to the injury site, have short half-lives in vivo , and could induce immunological response due to repeated administration (Wong, 2008). Potentiating regeneration of neurons without degrading the glial scar may be possible via the heparin-binding growth factor pleiotrophin (PTN).…”

Section: Introductionmentioning

confidence: 99%

Pleiotrophin signals through ALK receptor to enhance growth of neurons in the presence of inhibitory CSPGs

Gupta

Churchward

Todd

et al. 2022

Preprint

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Chondroitin sulfate proteoglycans (CSPGs), one of the major extracellular matrix components of the glial scar that surrounds central nervous system (CNS) injuries, are known to inhibit the regeneration of neurons. This study investigated whether pleiotrophin (PTN), a growth factor upregulated during early CNS development, can overcome the inhibition mediated by CSPGs and promote the neurite outgrowth of neurons in vitro. The data showed that a CSPG matrix inhibited the outgrowth of neurites in primary cortical neuron cultures compared to a control matrix. PTN elicited a dose dependent increase in the neurite outgrowth even in the presence of the growth inhibitory CSPG matrix, with optimal growth at 15 ng mL-1 of PTN (114.8% of neuronal outgrowth relative to laminin control). The growth promoting effect of PTN was blocked by inhibition of the receptor anaplastic lymphoma kinase (ALK) by alectinib in a dose dependent manner. Neurite outgrowth in the presence of this CSPG matrix was induced by activation of the protein kinase B (AKT) pathway, a key downstream mediator of ALK activation. This study identified PTN as a dose-dependent regulator of neurite outgrowth in primary cortical neurons cultured in the presence of a CSPG matrix, and identified ALK activation as a key driver of PTN-induced growth

show abstract

Knocking Down Glycosaminoglycan Synthesis

Cited by 2 publications

References 5 publications

Pleiotrophin Signals Through ALK Receptor to Enhance the Growth of Neurons in the Presence of Inhibitory Chondroitin Sulfate Proteoglycans

Pleiotrophin Signals Through ALK Receptor to Enhance the Growth of Neurons in the Presence of Inhibitory Chondroitin Sulfate Proteoglycans

Pleiotrophin signals through ALK receptor to enhance growth of neurons in the presence of inhibitory CSPGs

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