scholarly journals Effect of advanced glycation end products, extracellular matrix metalloproteinase inducer and matrix metalloproteinases on type-I collagen metabolism

2016 ◽  
Vol 4 (6) ◽  
pp. 691-693 ◽  
Author(s):  
WANG LI ◽  
WANG LING ◽  
XIAOMEI TENG ◽  
CUIXIA QUAN ◽  
SHENGNAN CAI ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinases ◽  
Matrix Metalloproteinase ◽  
Advanced Glycation End Products ◽  
Type I Collagen ◽  
Type I ◽  
Advanced Glycation ◽  
Extracellular Matrix Metalloproteinase Inducer ◽  
Glycation End Products ◽  
End Products

In VitroGlycoxidation of Insoluble Fibrous Type I Collagen: Solubilization and Advanced Glycation End Products

2003 ◽  
Vol 22 (6) ◽  
pp. 527-531 ◽  
Author(s):  
M. Meli ◽  
R. Granouillet ◽  
E. Reynaud ◽  
A. Chamson ◽  
J. Frey ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Type I Collagen ◽  
Type I ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Receptor for advanced glycation end-products (RAGE) is an indicator of direct lung injury in models of experimental lung injury

2009 ◽  
Vol 297 (1) ◽  
pp. L1-L5 ◽  
Author(s):  
Xiao Su ◽  
Mark R. Looney ◽  
Naveen Gupta ◽  
Michael A. Matthay
Keyword(s):  
Lung Injury ◽  
Advanced Glycation End Products ◽  
Cell Injury ◽  
Alveolar Epithelial Cell ◽  
Experimental Models ◽  
Alveolar Type ◽  
Type I ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Receptor for advanced glycation end-products (RAGE) is a marker of alveolar type I cells and is elevated in the pulmonary edema fluid of patients with acute lung injury (ALI). We tested the hypothesis that RAGE in the bronchoalveolar lavage (BAL) would be elevated in experimental models of direct ALI characterized by alveolar epithelial cell injury. We developed ELISA measurements for RAGE and studied ALI (direct and indirect) mouse models and collected BAL at specified endpoints to measure RAGE. We also tested whether levels of BAL RAGE correlated 1) with the severity of lung injury in acid and hyperoxia-induced ALI and 2) with the beneficial effect of a novel treatment, mesenchymal stem cells (MSC), in LPS-induced ALI. In ALI models of direct lung injury induced by intratracheal instillation of acid, LPS, or Escherichia coli, the BAL RAGE was 58-, 22-, and 13-fold elevated, respectively. In contrast, BAL RAGE was not detectable in indirect models of ALI induced by an intraperitoneal injection of thiourea or by an intravenous injection of MHC I monoclonal antibody that produces a mouse model of transfusion-related ALI. BAL RAGE did correlate with the severity of lung injury in acid and hyperoxia-induced ALI. In addition, with LPS-induced ALI, BAL RAGE was markedly reduced with MSC treatment. In summary, BAL RAGE is an indicator of ALI, and it may be useful in distinguishing direct from indirect models of ALI as well as assessing the response to specific therapies.

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

2019 ◽  
Author(s):  
Shivam H. Patel ◽  
Feng Yue ◽  
Shannon K. Saw ◽  
Rachel Foguth ◽  
Jason R. Cannon ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Achilles Tendon ◽  
Advanced Glycation End Products ◽  
Mitochondrial Function ◽  
Diabetic Patients ◽  
Proliferative Capacity ◽  
Advanced Glycation ◽  
Tendon Degeneration ◽  
Glycation End Products ◽  
End Products

AbstractDebilitating 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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