Basic Study
Copyright ©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Stem Cells. Jul 26, 2020; 12(7): 621-632
Published online Jul 26, 2020. doi: 10.4252/wjsc.v12.i7.621
Involvement of glycated albumin in adipose-derived-stem cell-mediated interleukin 17 secreting T helper cell activation
Julien Pestel, Maud Robert, Sara Corbin, Hubert Vidal, Assia Eljaafari
Julien Pestel, Maud Robert, Hubert Vidal, Assia Eljaafari, INSERM U1060 CarMen, Batiment CENS-ELI, Centre Hospitalier Lyon Sud, Pierre Bénite 69310, France
Julien Pestel, Maud Robert, Hubert Vidal, Assia Eljaafari, Faculty of Medicine, Université Claude Bernard Lyon 1, Batiment CENS-ELI, Centre Hospitalier Lyon Sud, Pierre Bénite 69310, France
Maud Robert, Department of Surgery in Gastro-enterology, Edouard Herriot Hospital, Lyon 69003, France
Sara Corbin, Public Health Department, Hospices Civils de Lyon, 1 quai des célestins Lyon 69002, France
Assia Eljaafari, DO-IT Research Team, Hospices Civils de Lyon, 1 quai des célestins, Lyon 69002, France
Author contributions: Pestel J performed the experiments, acquired and analyzed data and was involved in data interpretation and in the writing of the manuscript; Robert M provided the residual adipose tissues and participated in the writing of the manuscript; Corbin S supervised the statistical data and helped in the revision of the manuscript; Vidal H participated in the design of the study, data interpretation, and writing of the manuscript; Eljaafari A designed, coordinated the study, was involved in data interpretation and in the writing of the manuscript. All authors approved the final version of the article.
Institutional review board statement: All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The Committee for people Protection emanating from the Research Ministry, has given us its approval for the use of human adipose tissues isolated from residues of visceral surgery. Informed consents were signed by each donor.
Conflict-of-interest statement: No potential conflicts of interest were disclosed.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Assia Eljaafari, MD, PhD, Doctor, Senior Scientist, CarMeN Laboratory, INSERM U1060, University Claude Bernard Lyon 1 and Hospices Civils de Lyon, Batiment CENS-ELI, Centre Hospitalier Lyon Sud, 165 chemin du Grand Revoyet, Pierre Bénite 69310, France. assia.eljaafari@univ-lyon1.fr
Received: February 28, 2020
Peer-review started: February 28, 2020
First decision: April 18, 2020
Revised: May 19, 2020
Accepted: June 10, 2020
Article in press: June 10, 2020
Published online: July 26, 2020
Processing time: 148 Days and 10.1 Hours
Core Tip

Core tip: Using a coculture model with human lean adipose-derived stem cells (ASC) and mononuclear cells, we have shown in this study that glycated human serum albumin (G-HSA) enhances lean ASC-mediated interleukin (IL)-17A, interferon gamma and tumor necrosis factor alpha secretion. This effect involved the advanced glycated end products (AGE)/Receptor of advanced glycated end products (RAGE) axis as assessed by anti-RAGE blocking antibodies and was associated with increased expression of RAGE and human leukocyte antigen-DR molecules. Thus, our results demonstrated that G-HSA potentiated lean ASC-mediated IL-17A production in adipose tissues, suggesting a new mechanism by which AGE could contribute to type 1 diabetes pathophysiology.