Antioxidants Reverse the Antiproliferative Effect of High Glucose and Advanced Glycosylation End Products in Cultured Rat Mesangial Cells

1994 ◽  
Vol 199 (1) ◽  
pp. 346-352 ◽  
Author(s):  
H. Trachtman ◽  
S. Futterweit ◽  
J. Prenner ◽  
S. Hanon
Keyword(s):  
High Glucose ◽  
Mesangial Cells ◽  
Antiproliferative Effect ◽  
Advanced Glycosylation End Products ◽  
End Products ◽  
Advanced Glycosylation

scholarly journals PDGF and TGF-β mediate collagen production by mesangial cells exposed to advanced glycosylation end products

1995 ◽  
Vol 48 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Douglas C. Throckmorton ◽  
Anne P. Brogden ◽  
Brian Min ◽  
Howard Rasmussen ◽  
Michael Kashgarian
Keyword(s):  
Mesangial Cells ◽  
Collagen Production ◽  
Advanced Glycosylation End Products ◽  
End Products ◽  
Advanced Glycosylation

scholarly journals Hyperglycemia-induced accumulation of advanced glycosylation end products in fibroblast-like synoviocytes promotes knee osteoarthritis

2021 ◽  
Author(s):  
Qingxian Li ◽  
Yinxian Wen ◽  
Linlong Wang ◽  
Biao Chen ◽  
Jun Chen ◽  
...  
Keyword(s):  
High Glucose ◽  
Glucose Transporter ◽  
Critical Role ◽  
Inflammatory Factors ◽  
Glucose Transporter 1 ◽  
Advanced Glycosylation End Products ◽  
End Products ◽  
Advanced Glycosylation ◽  
Fibroblast Like Synoviocytes

AbstractOsteoarthritis (OA) is significantly associated with diabetes, but how hyperglycemia induces or aggravates OA has not been shown. The synovium plays a critical role in cartilage metabolism and substance exchange. Herein, we intended to investigate whether and how hyperglycemia affects the occurrence and progression of OA by influencing the synovium. In patients with knee OA and diabetes (DM OA), we found a more severe inflammatory response, higher endoplasmic reticulum stress (ERS) levels, and more advanced glycosylation end products (AGEs) accumulation in the synovium than in patients without diabetes. Subsequently, we found similar results in the DM OA group in a rat model. In the in vitro cocultivation system, high glucose-stimulated AGEs accumulation, ERS, and inflammation in rat fibroblast-like synoviocytes (FLSs), which resulted in chondrocyte degeneration due to inflammatory factors from FLSs. Furthermore, in the synovium of the DM OA group and FLSs treated with high glucose, the expression of glucose transporter 1 (GLUT1) and its regulatory factor hypoxia-inducible factor (HIF)-1α was increased significantly. Inhibitors of HIF-1α, GLUT1 or AGEs receptors attenuated the effect of high glucose on chondrocyte degradation in the FLS-chondrocyte coculture system. In summary, we demonstrated that hyperglycemia caused AGEs accumulation in FLSs via the HIF-1α-GLUT1 pathway, which increases the release of inflammatory factors from FLSs, subsequently inducing chondrocyte degradation and promoting OA progression.

scholarly journals Influences of advanced glycosylation end products on the inner blood–retinal barrier in a co-culture cell model in vitro

2020 ◽  
Vol 15 (1) ◽  
pp. 619-628
Author(s):  
Chen Yuan ◽  
Ya Mo ◽  
Jie Yang ◽  
Mei Zhang ◽  
Xuejun Xie
Keyword(s):  
Electrical Resistance ◽  
Cell Model ◽  
Polyclonal Antibodies ◽  
Time Dependent ◽  
Dependent Manner ◽  
Blood Retinal Barrier ◽  
Advanced Glycosylation End Products ◽  
End Products ◽  
Advanced Glycosylation

AbstractAdvanced glycosylation end products (AGEs) are harmful factors that can damage the inner blood–retinal barrier (iBRB). Rat retinal microvascular endothelial cells (RMECs) were isolated and cultured, and identified by anti-CD31 and von Willebrand factor polyclonal antibodies. Similarly, rat retinal Müller glial cells (RMGCs) were identified by H&E staining and with antibodies of glial fibrillary acidic protein and glutamine synthetase. The transepithelial electrical resistance (TEER) value was measured with a Millicell electrical resistance system to observe the leakage of the barrier. Transwell cell plates for co-culturing RMECs with RMGCs were used to construct an iBRB model, which was then tested with the addition of AGEs at final concentrations of 50 and 100 mg/L for 24, 48, and 72 h. AGEs in the in vitro iBRB model constructed by RMEC and RMGC co-culture led to the imbalance of the vascular endothelial growth factor (VEGF) and pigment epithelial derivative factor (PEDF), and the permeability of the RMEC layer increased because the TEER decreased in a dose- and time-dependent manner. AGEs increased VEGF but lowered PEDF in a dose- and time-dependent manner. The intervention with AGEs led to the change of the transendothelial resistance of the RMEC layer likely caused by the increased ratio of VEGF/PEDF.

Advanced Glycosylation End Products in Patients with Diabetic Nephropathy

1991 ◽  
Vol 325 (12) ◽  
pp. 836-842 ◽  
Author(s):  
Zenji Makita ◽  
Steven Radoff ◽  
Elliot J. Rayfield ◽  
Zhi Yang ◽  
Edward Skolnik ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycosylation End Products ◽  
End Products ◽  
Advanced Glycosylation
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