Next Article in Journal
Insight into the Structural Determinants of Imidazole Scaffold-Based Derivatives as TNF-α Release Inhibitors by in Silico Explorations
Next Article in Special Issue
Th17 Cells as Potential Probiotic Therapeutic Targets in Inflammatory Bowel Diseases
Previous Article in Journal
Highlight: Mitochondrial Mechanisms in Septic Cardiomyopathy
Previous Article in Special Issue
New Immunosuppressive Therapies in Uveitis Treatment
Article

AGEs-Induced IL-6 Synthesis Precedes RAGE Up-Regulation in HEK 293 Cells: An Alternative Inflammatory Mechanism?

1
Department of Preclinical Sciences, Faculty of Veterinary Medicine, University of Agronomical Sciences and Veterinary Medicine Bucharest, 105 Splaiul Independentei, district 5, Bucharest 050097, Romania
2
Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Bucharest, 91–95 Splaiul Independentei, district 5, Bucharest 050095, Romania
*
Author to whom correspondence should be addressed.
Academic Editor: Kamal D. Moudgil
Int. J. Mol. Sci. 2015, 16(9), 20100-20117; https://doi.org/10.3390/ijms160920100
Received: 27 April 2015 / Revised: 12 June 2015 / Accepted: 6 August 2015 / Published: 25 August 2015
(This article belongs to the Special Issue Mechanism of Action and Applications of Cytokines in Immunotherapy)
Advanced glycation end products (AGEs) can activate the inflammatory pathways involved in diabetic nephropathy. Understanding these molecular pathways could contribute to therapeutic strategies for diabetes complications. We evaluated the modulation of inflammatory and oxidative markers, as well as the protective mechanisms employed by human embryonic kidney cells (HEK 293) upon exposure to 200 μg/mL bovine serum albumine (BSA) or AGEs–BSA for 12, 24 and 48 h. The mRNA and protein expression levels of AGEs receptor (RAGE) and heat shock proteins (HSPs) 27, 60 and 70, the activity of antioxidant enzymes and the expression levels of eight cytokines were analysed. Cell damage via oxidative mechanisms was evaluated by glutathione and malondialdehyde levels. The data revealed two different time scale responses. First, the up-regulation of interleukin-6 (IL-6), HSP 27 and high catalase activity were detected as early as 12 h after exposure to AGEs–BSA, while the second response, after 24 h, consisted of NF-κB p65, RAGE, HSP 70 and inflammatory cytokine up-regulation, glutathione depletion, malondialdehyde increase and the activation of antioxidant enzymes. IL-6 might be important in the early ignition of inflammatory responses, while the cellular redox imbalance, RAGE activation and NF-κB p65 increased expression further enhance inflammatory signals in HEK 293 cells. View Full-Text
Keywords: advanced glycation end products; heat-shock proteins; HEK 293 cells; inflammation; oxidative stress advanced glycation end products; heat-shock proteins; HEK 293 cells; inflammation; oxidative stress
Show Figures

Graphical abstract

MDPI and ACS Style

Serban, A.I.; Stanca, L.; Geicu, O.I.; Dinischiotu, A. AGEs-Induced IL-6 Synthesis Precedes RAGE Up-Regulation in HEK 293 Cells: An Alternative Inflammatory Mechanism? Int. J. Mol. Sci. 2015, 16, 20100-20117. https://doi.org/10.3390/ijms160920100

AMA Style

Serban AI, Stanca L, Geicu OI, Dinischiotu A. AGEs-Induced IL-6 Synthesis Precedes RAGE Up-Regulation in HEK 293 Cells: An Alternative Inflammatory Mechanism? International Journal of Molecular Sciences. 2015; 16(9):20100-20117. https://doi.org/10.3390/ijms160920100

Chicago/Turabian Style

Serban, Andreea I.; Stanca, Loredana; Geicu, Ovidiu I.; Dinischiotu, Anca. 2015. "AGEs-Induced IL-6 Synthesis Precedes RAGE Up-Regulation in HEK 293 Cells: An Alternative Inflammatory Mechanism?" Int. J. Mol. Sci. 16, no. 9: 20100-20117. https://doi.org/10.3390/ijms160920100

Find Other Styles

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Search more from Scilit
 
Search
Back to TopTop