RAGE Mediates Cholesterol Efflux Impairment in Macrophages Caused by Human Advanced Glycated Albumin

Overview

Journal Int J Mol Sci

Publisher MDPI

Specialties Biochemistry
Chemistry
Molecular Biology

Date 2020 Oct 6

PMID 33019603

Citations 11

Authors

Adriana Machado-Lima

Raquel Lopez-Diez

Rodrigo Tallada Iborra

Raphael de Souza Pinto

Gurdip Daffu

Xiaoping Shen

Edna Regina Nakandakare

Ubiratan Fabres Machado

Maria Lucia Cardillo Correa-Giannella

Ann Marie Schmidt

Marisa Passarelli

Affiliations

Soon will be listed here.

Abstract

We addressed the involvement of the receptor for advanced glycation end products (RAGE) in the impairment of the cellular cholesterol efflux elicited by glycated albumin. Albumin was isolated from type 1 (DM1) and type 2 (DM2) diabetes mellitus (HbA1c > 9%) and non-DM subjects (C). Moreover, albumin was glycated in vitro (AGE-albumin). Macrophages from null and wild-type (WT) mice, or THP-1 transfected with siRNA- were treated with C, DM1, DM2, non-glycated or AGE-albumin. The cholesterol efflux was reduced in WT cells exposed to DM1 or DM2 albumin as compared to C, and the intracellular lipid content was increased. These events were not observed in null cells, in which the cholesterol efflux and lipid staining were, respectively, higher and lower when compared to WT cells. In WT, , and mRNA increased and and diminished after treatment with DM1 and DM2 albumin. In null cells treated with DM-albumin, , and were reduced and and increased. In -silenced THP-1, and mRNA were reduced and and were increased even after treatment with AGE or DM-albumin. RAGE mediates the deleterious effects of AGE-albumin in macrophage cholesterol efflux.

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