subject:(Chondroitinase ABC)

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University of California – San Diego

1. Liang, Justine. Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment.

Degree: Biology, 2016, University of California – San Diego

URL: http://www.escholarship.org/uc/item/02t8c2w9

Several factors contribute to the lack of repair following spinal cord injury, such as the lack of growth-promoting factors, poor intrinsic central nervous system regeneration abilities, and inhibition due to the glial scar1. The glial scar contains a class of inhibitory extracellular matrix molecules, chondroitin sulfate proteoglycans (CSPGs), which create a physical and chemical barrier to axon regeneration and sprouting. Previous studies showed that administration of an enzyme, chondroitinase ABC (ch'ase), can remove this inhibition and promote functional and behavioral recovery in smaller animal models. To aid in translation to clinical trials, we examined whether ch'ase administration in a rhesus monkey model of spinal cord injury promoted such recovery. As of now, 9 of the 12 subjects were analyzed and we found a trend towards anatomical and behavioral recovery in ch'ase administered subjects. The trend toward increased corticospinal tract sprouting in ch’ase subjects may demonstrate that the success of ch’ase in smaller animal models is not unfounded. However, the behavioral recovery is not as distinct, and perhaps more optimization of ch’ase treatment is required in the monkey model before translation to clinical trials. Further conclusions can be drawn once the remaining 3 subjects have been analyzed and assessed. However, despite the incomplete dataset and low n, there are interesting trends in the data that may influence whether the ch’ase treatment will move on to clinical trials.

Subjects/Keywords: Neurosciences; Biology; axonal sprouting; chondroitinase ABC; chondroitin sulfate proteoglycan; corticospinal tract; rhesus monkey; spinal cord injury

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APA (6^th Edition):

Liang, J. (2016). Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/02t8c2w9

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Liang, Justine. “Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment.” 2016. Thesis, University of California – San Diego. Accessed February 25, 2021. http://www.escholarship.org/uc/item/02t8c2w9.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Liang, Justine. “Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment.” 2016. Web. 25 Feb 2021.

Vancouver:

Liang J. Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment. [Internet] [Thesis]. University of California – San Diego; 2016. [cited 2021 Feb 25]. Available from: http://www.escholarship.org/uc/item/02t8c2w9.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liang J. Chondroitinase ABC Administration in a Non-Human Primate Model of Spinal Cord Injury: Functional and Anatomical Assessment. [Thesis]. University of California – San Diego; 2016. Available from: http://www.escholarship.org/uc/item/02t8c2w9

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Rice University

2. Natoli, Roman M. Impact loading and functional tissue engineering of articular cartilage.

Degree: PhD, Engineering, 2009, Rice University

URL: http://hdl.handle.net/1911/88472

This thesis presents two advances for alleviating the problem of articular cartilage degeneration: mitigating degradative changes that follow mechanically induced injuries and growing functional neo-cartilage for diseased tissue replacement. Experiments demonstrate that cartilage subjected to a single, non-surface disrupting 1.1 J (Low) impact experiences sufficient degeneration over 4 weeks to become functionally equivalent to tissue subjected to a single, surface disrupting 2.8 J (High) impact. By 24 hrs post High impact, cell death and sulfated glycosaminoglycan (sGAG) release increased, changes in gene expression distinguished injured from adjacent tissue, and compressive stiffness decreased. In contrast, Low impacted tissue did not show decreased compressive stiffness until 4 weeks, revealing that Low impacted tissue experiences a delayed biological response. Post-injury treatment with the polymer P188, growth factor IGF-I, or matrix metalloproteinase inhibitor doxycycline partially ameliorated cell death and sGAG loss, two detrimental changes that occurred following either Low or High impact. With 1 week of treatment after Low impact, P188 reduced cell death 75% and IGF-I decreased sGAG release 49%. Following High impact, doxycycline treatment reduced 1 and 2 week sGAG release by 30% and 38%, respectively. As a novel method for engineering functional replacement tissue to use in cases of established disease, the GAG degrading enzyme chondroitinase ABC (C-ABC) improved the tensile integrity of articular cartilage constructs grown with a scaffold-less approach. C-ABC application increased ultimate tensile strength and tensile stiffness, reaching values of 1.4 and 3.4 MPa, respectively. Moreover, construct collagen concentration was ∼22% by wet weight. Though C-ABC temporarily depleted sGAG, by 6 weeks no significant differences in compressive stiffness remained. Furthermore, chondrocyte phenotype was maintained, as constructs contained collagen type II, but not collagen type I. Decorin decreased following C-ABC treatment, but recovered during subsequent culture. The known ability of decorin to control collagen fibrillogenesis suggests a putative mechanism for C-ABC's effects. Diseased articular cartilage heals poorly. For patients, the last resort is total joint replacement, though its associated morbidity and the limited lifespan of its results drive the need for alternate treatment strategies. Decreasing degradative changes post-injury and increasing functional properties of engineered cartilage are two significant improvements. Advisors/Committee Members: Athanasiou, Kyriacos (advisor), Grande-Allen, Jane (committee member), Gustin, Michael (committee member).

Subjects/Keywords: Biomedical engineering; Medicine; Physiology; Health and environmental sciences; Applied sciences; Biological sciences; Tissue engineering; Articular cartilage; Mechanobiology; Biomechanics; Mechanotransduction; Osteoarthritis; Chondroitinase ABC

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Natoli, R. M. (2009). Impact loading and functional tissue engineering of articular cartilage. (Doctoral Dissertation). Rice University. Retrieved from http://hdl.handle.net/1911/88472

Chicago Manual of Style (16^th Edition):

Natoli, Roman M. “Impact loading and functional tissue engineering of articular cartilage.” 2009. Doctoral Dissertation, Rice University. Accessed February 25, 2021. http://hdl.handle.net/1911/88472.

MLA Handbook (7^th Edition):

Natoli, Roman M. “Impact loading and functional tissue engineering of articular cartilage.” 2009. Web. 25 Feb 2021.

Vancouver:

Natoli RM. Impact loading and functional tissue engineering of articular cartilage. [Internet] [Doctoral dissertation]. Rice University; 2009. [cited 2021 Feb 25]. Available from: http://hdl.handle.net/1911/88472.

Council of Science Editors:

Natoli RM. Impact loading and functional tissue engineering of articular cartilage. [Doctoral Dissertation]. Rice University; 2009. Available from: http://hdl.handle.net/1911/88472

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