Controlled release of neurotrophin-3 from fibrin-based tissue engineering scaffolds enhances neural fiber sprouting following subacute spinal cord injury

This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-e...

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Published inBiotechnology and bioengineering Vol. 104; no. 6; pp. 1207 - 1214
Main Authors Johnson, Philip J, Parker, Stanley R, Sakiyama-Elbert, Shelly E
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 15.12.2009
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Abstract This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin-based delivery system with different concentrations of NT-3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT-3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT-3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury. Biotechnol. Bioeng. 2009; 104: 1207-1214.
AbstractList Abstract This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin‐3 (NT‐3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re‐exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin‐based delivery system with different concentrations of NT‐3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT‐3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT‐3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT‐3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury. Biotechnol. Bioeng. 2009; 104: 1207–1214. © 2009 Wiley Periodicals, Inc.
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin-based delivery system with different concentrations of NT-3 (500 and 1000 ng/mL), or a fibrin scaffold containing 1000 ng/mL of NT-3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT-3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury.
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin‐3 (NT‐3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re‐exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin‐based delivery system with different concentrations of NT‐3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT‐3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT‐3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT‐3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury. Biotechnol. Bioeng. 2009; 104: 1207–1214. © 2009 Wiley Periodicals, Inc.
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin-based delivery system with different concentrations of NT-3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT-3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT-3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury. Biotechnol. Bioeng. 2009; 104: 1207-1214.
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin-based delivery system with different concentrations of NT-3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT-3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT-3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury.
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate enhanced neural fiber sprouting. Long Evans rats received a T9 dorsal hemisection spinal cord injury. Two weeks later, the injury site was re-exposed, and either a fibrin scaffold alone, a fibrin scaffold containing a heparin-based delivery system with different concentrations of NT-3 (500 and 1,000 ng/mL), or a fibrin scaffold containing 1,000 ng/mL of NT-3 (no delivery system) was implanted into the injury site. The injured spinal cords were evaluated for morphological differences using markers for neurons, astrocytes, and chondroitin sulfate proteoglycans 2 weeks after treatment. The addition of 500 ng/mL of NT-3 with the delivery system resulted in an increase in neural fiber density compared to fibrin alone. These results demonstrate that the controlled release of NT-3 from fibrin scaffolds can enhance neural fiber sprouting even when treatment is delayed 2 weeks following injury. [PUBLICATION ABSTRACT]
Author Parker, Stanley R
Sakiyama-Elbert, Shelly E
Johnson, Philip J
AuthorAffiliation 2 Division of Plastic and Reconstructive Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA
3 Center for Materials Innovation, Washington University, St. Louis, MO 63130, USA
1 Department of Biomedical Engineering, Washington University, St. Louis, MO 63130, USA
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Issue 6
Keywords Neurotrophin
Delivery system
growth factors
Tissue engineering
Fiber
Nerve
Fibrin
Regeneration
Spinal cord trauma
Biomaterial
nerve regeneration
Release
Growth factor
Language English
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Publisher Wiley Subscription Services, Inc., A Wiley Company
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Snippet This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin-3 (NT-3) from fibrin scaffolds can stimulate...
This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin‐3 (NT‐3) from fibrin scaffolds can stimulate...
Abstract This study investigated whether delayed treatment of spinal cord injury with controlled release of neurotrophin‐3 (NT‐3) from fibrin scaffolds can...
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StartPage 1207
SubjectTerms Animals
Biological and medical sciences
biomaterial
Biotechnology
delivery system
Female
Fibrin
Fundamental and applied biological sciences. Psychology
growth factors
Medical treatment
Nerve Fibers - drug effects
Nerve Regeneration
Neurons
Neurotrophin 3 - pharmacokinetics
Rats
Rats, Long-Evans
Rodents
Spinal Cord - pathology
Spinal cord injuries
Spinal Cord Injuries - therapy
Studies
Tissue Engineering - methods
Tissue Scaffolds - chemistry
Title Controlled release of neurotrophin-3 from fibrin-based tissue engineering scaffolds enhances neural fiber sprouting following subacute spinal cord injury
URI https://api.istex.fr/ark:/67375/WNG-L34MC1HT-2/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fbit.22476
https://www.ncbi.nlm.nih.gov/pubmed/19603426
https://www.proquest.com/docview/213760621
https://search.proquest.com/docview/743658319
https://search.proquest.com/docview/746080130
https://pubmed.ncbi.nlm.nih.gov/PMC2780336
Volume 104
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