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 in | Biotechnology and bioengineering Vol. 104; no. 6; pp. 1207 - 1214 |
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Format | Journal Article |
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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. |
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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 |
AuthorAffiliation_xml | – name: 2 Division of Plastic and Reconstructive Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, MO 63110, USA – name: 3 Center for Materials Innovation, Washington University, St. Louis, MO 63130, USA – name: 1 Department of Biomedical Engineering, Washington University, St. Louis, MO 63130, USA |
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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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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 |
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