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The Role of Glycosaminoglycans in Fatigue Injured Tendon.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The Role of Glycosaminoglycans in Fatigue Injured Tendon./
作者:	Muljadi, Patrick Mahardhika.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2022,
面頁冊數:	97 p.
附註:	Source: Dissertations Abstracts International, Volume: 83-12, Section: B.
Contained By:	Dissertations Abstracts International83-12B.
標題:	Biomedical engineering. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=29069223
ISBN:	9798819368008

The Role of Glycosaminoglycans in Fatigue Injured Tendon.
Muljadi, Patrick Mahardhika.

The Role of Glycosaminoglycans in Fatigue Injured Tendon. - Ann Arbor : ProQuest Dissertations & Theses, 2022 - 97 p.

Source: Dissertations Abstracts International, Volume: 83-12, Section: B.

Thesis (Ph.D.)--Cornell University, 2022.

This item must not be sold to any third party vendors.

This dissertation reviews how tendon overuse injuries disrupt the extracellular matrix (ECM) and its interactions with cells at multiple scales, influencing repair after injury and suggesting that therapeutics for tendinopathy should be assessed with consideration of their effects on the ECM and its role in mechanotransduction. Utilizing our fatigue loading model of early-onset, subrupture tendinopathy, we characterized bulk and location specific increases in glycosaminoglycans (GAGs), including increased decorin-associated dermatan sulfate in the midsubstance ECM and increased chondroitin sulfate and hyaluronic acid in the pericellular matrix after fatigue injury. We hypothesized that the increase in GAGs with fatigue injury is a key contributor to tendon mechanical properties, mechanotransduction, and repair in response to exercise. When we removed the increased GAGs from fatigue injured tendons by ex vivo enzymatic treatment, we observed increased microscale strain, reduced dynamic modulus, and increased loss tangent relative to naive control tendons. When we continuously reduced GAGs in vivo after fatigue injury, we observed an increase in tenomodulin, decreased loss tangent in the toe region, and increased loss tangent in the linear region, consistent with ex vivo GAG removal. These findings demonstrate a role for post-injury GAGs in directly and indirectly modulating multiscale mechanics and viscoelasticity as well as limiting tenogenic phenotype. Clinically, GAGs could serve as a diagnostic or therapeutic target to modulate mechanotransduction and enable reparative exercise after fatigue injury and tendinopathy.

ISBN: 9798819368008Subjects--Topical Terms:

535387
Biomedical engineering.
Subjects--Index Terms:

Extracellular Matrix

The Role of Glycosaminoglycans in Fatigue Injured Tendon.
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500 $a Source: Dissertations Abstracts International, Volume: 83-12, Section: B.
500 $a Advisor: Andarawis-Puri, Nelly.
502 $a Thesis (Ph.D.)--Cornell University, 2022.
506 $a This item must not be sold to any third party vendors.
520 $a This dissertation reviews how tendon overuse injuries disrupt the extracellular matrix (ECM) and its interactions with cells at multiple scales, influencing repair after injury and suggesting that therapeutics for tendinopathy should be assessed with consideration of their effects on the ECM and its role in mechanotransduction. Utilizing our fatigue loading model of early-onset, subrupture tendinopathy, we characterized bulk and location specific increases in glycosaminoglycans (GAGs), including increased decorin-associated dermatan sulfate in the midsubstance ECM and increased chondroitin sulfate and hyaluronic acid in the pericellular matrix after fatigue injury. We hypothesized that the increase in GAGs with fatigue injury is a key contributor to tendon mechanical properties, mechanotransduction, and repair in response to exercise. When we removed the increased GAGs from fatigue injured tendons by ex vivo enzymatic treatment, we observed increased microscale strain, reduced dynamic modulus, and increased loss tangent relative to naive control tendons. When we continuously reduced GAGs in vivo after fatigue injury, we observed an increase in tenomodulin, decreased loss tangent in the toe region, and increased loss tangent in the linear region, consistent with ex vivo GAG removal. These findings demonstrate a role for post-injury GAGs in directly and indirectly modulating multiscale mechanics and viscoelasticity as well as limiting tenogenic phenotype. Clinically, GAGs could serve as a diagnostic or therapeutic target to modulate mechanotransduction and enable reparative exercise after fatigue injury and tendinopathy.
590 $a School code: 0058.
650 4 $a Biomedical engineering. $3 535387
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650 4 $a Biomechanics. $3 548685
650 4 $a Physiology. $3 518431
650 4 $a Physical therapy. $3 588713
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653 $a Overuse injury
653 $a Tendinopathy
653 $a Tendon repair
653 $a Mechanotransduction
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