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Advanced Glycation End-Products Suppress Mitochondrial Function and Proliferative Capacity of Achilles Tendon-Derived Fibroblasts

Shivam H. Patel, Feng Yue, Shannon K. Saw, Rachel Foguth, Jason R. Cannon, Jonathan H. Shannahan, Shihuan Kuang, Arman Sabbaghi, Chad C. Carroll
doi: https://doi.org/10.1101/706754
Shivam H. Patel
Department of Health and Kinesiology, Purdue University, West Lafayette, IN
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Feng Yue
Department of Animal Sciences, Purdue University, West Lafayette, IN
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Shannon K. Saw
Department of Health and Kinesiology, Purdue University, West Lafayette, IN
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Rachel Foguth
School of Health Sciences, Purdue University, West Lafayette, INPurdue Institute for Integrative Neuroscience, West Lafayette, IN
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Jason R. Cannon
School of Health Sciences, Purdue University, West Lafayette, INPurdue Institute for Integrative Neuroscience, West Lafayette, IN
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Jonathan H. Shannahan
School of Health Sciences, Purdue University, West Lafayette, IN
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Shihuan Kuang
Department of Animal Sciences, Purdue University, West Lafayette, IN
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Arman Sabbaghi
Department of Statistics, Purdue University, West Lafayette, IN
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Chad C. Carroll
Department of Health and Kinesiology, Purdue University, West Lafayette, INIndiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN
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  • For correspondence: carrol71@purdue.edu
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Abstract

Debilitating cases of tendon pain and degeneration affect the majority of diabetic individuals. The high rate of tendon degeneration persists even when glucose levels are well controlled, suggesting that other mechanisms may drive tendon degeneration in diabetic patients. The purpose of this study was to investigate the impact of advanced glycation end-products on tendon fibroblasts to further our mechanistic understanding of the development and progression of diabetic tendinopathy. We proposed that advanced glycation end-products would induce limitations to mitochondrial function and proliferative capacity in tendon-derived fibroblasts, restricting their ability to maintain biosynthesis of tendon extracellular matrix. Using an in-vitro cell culture system, rat Achilles tendon fibroblasts were treated with glycolaldehyde-derived advanced glycation end-products (0, 50, 100, and 200μg/ml) for 48 hours in normal glucose (5.5mM) and high glucose (25mM) conditions. We demonstrate that tendon fibroblasts treated with advanced glycation end-products display reduced ATP production, electron transport efficiency, and proliferative capacity. These impairments were coupled with alterations in mitochondrial DNA content and expression of genes associated with extracellular matrix remodeling, mitochondrial energy metabolism, and apoptosis. Our findings suggest that advanced glycation end-products disrupt tendon fibroblast homeostasis and may be involved in the development and progression of diabetic tendinopathy.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted July 18, 2019.
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Advanced Glycation End-Products Suppress Mitochondrial Function and Proliferative Capacity of Achilles Tendon-Derived Fibroblasts
Shivam H. Patel, Feng Yue, Shannon K. Saw, Rachel Foguth, Jason R. Cannon, Jonathan H. Shannahan, Shihuan Kuang, Arman Sabbaghi, Chad C. Carroll
bioRxiv 706754; doi: https://doi.org/10.1101/706754
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Advanced Glycation End-Products Suppress Mitochondrial Function and Proliferative Capacity of Achilles Tendon-Derived Fibroblasts
Shivam H. Patel, Feng Yue, Shannon K. Saw, Rachel Foguth, Jason R. Cannon, Jonathan H. Shannahan, Shihuan Kuang, Arman Sabbaghi, Chad C. Carroll
bioRxiv 706754; doi: https://doi.org/10.1101/706754

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