High glucose and hyperglycemic sera from type 2 diabetic patients impair DC differentiation by inducing ROS and activating Wnt/β-catenin and p38 MAPK
详细信息 查看全文
- 作者：Maria Saveria Gilardini Montania ; Marisa Granatoa ; Laura Cuomob ; Sandro Valiaa ; Livia Di Renzoa ; Gabriella D'Orazic ; d ; Alberto Faggionia ; alberto.faggioni@uniroma1.it" class="auth_mail" title="E-mail the corresponding author ; Mara Cironea ; mara.cirone@uniroma1.it" class="auth_mail" title="E-mail the corresponding author
- 关键词：DCs ; dendritic cells ; DM2 ; type 2 diabetes ; ROS ; reactive oxygen species ; MAPKs ; mitogen-activated protein kinases ; PAMPs ; pathogen associated molecular patterns ; DAMPs ; damage associated molecular patterns ; TCF/LEF ; T-cell factor/lymphoid enhancer factor ; ERKs ; extracellular regulated kinase? ; JNKs ; c-Jun N-terminal kinases ; HG ; high glucose ; HYG ; hyperglycemic sera ; NG ; normoglycemic sera ; PEL ; primary effusion lymphoma ; Q ; quercetin ; DCFDA ; 2&prime ; 7&prime ; -dichlorofluorescein diacetate ; IL-
- 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- 出版年：2016
- 出版时间：April 2016
- 年：2016
- 卷：1862
- 期：4
- 页码：805-813
- 全文大小：1469 K
文摘
- •
High glucose and hyperglycemic sera from type 2 diabetic patients impair DC differentiation and maturation.
- •
High glucose and hyperglycemic sera increase ROS production and activate Wnt/β-catenin and p38 MAPK pathways in dysfunctional iDCs.
- •
Quercetin partially reverts the immune-suppressive effects mediated by high glucose and by hyperglycemic sera.