Role of the Scavenger Receptor CD36 in Accelerated Diabetic Atherosclerosis
Navas Madroñal, Miquel (Institut d'Investigació Biomèdica Sant Pau)
Castelblanco, Esmeralda (Institut d'Investigació Biomèdica Sant Pau)
Camacho, Mercedes (Institut d'Investigació Biomèdica Sant Pau)
Consegal, Marta (Institut d'Investigació Biomèdica Sant Pau)
Ramírez-Morros, Anna (Institut Germans Trias i Pujol)
Sarrias, Maria-Rosa (Institut Germans Trias i Pujol)
Perez, Paulina (Institut Germans Trias i Pujol. Hospital Universitari Germans Trias i Pujol)
Alonso Pedrol, Núria (Institut Germans Trias i Pujol)
Galán, María (Institut d'Investigació Biomèdica Sant Pau)
Mauricio Puente, Dídac (Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas)
Universitat Autònoma de Barcelona

Date:	2020
Abstract:	Diabetes mellitus entails increased atherosclerotic burden and medial arterial calcification, but the precise mechanisms are not fully elucidated. We aimed to investigate the implication of CD36 in inflammation and calcification processes orchestrated by vascular smooth muscle cells (VSMCs) under hyperglycemic and atherogenic conditions. We examined the expression of CD36, pro-inflammatory cytokines, endoplasmic reticulum (ER) stress markers, and mineralization-regulating enzymes by RT-PCR in human VSMCs, cultured in a medium containing normal (5 mM) or high glucose (22 mM) for 72 h with or without oxidized low-density lipoprotein (oxLDL) (24 h). The uptake of 1,1'-dioctadecyl-3,3,3',3-tetramethylindocarbocyanine perchlorate-fluorescently (DiI) labeled oxLDL was quantified by flow cytometry and fluorimetry and calcification assays were performed in VSMC cultured in osteogenic medium and stained by alizarin red. We observed induction in the expression of CD36, cytokines, calcification markers, and ER stress markers under high glucose that was exacerbated by oxLDL. These results were confirmed in carotid plaques from subjects with diabetes versus non-diabetic subjects. Accordingly, the uptake of DiI-labeled oxLDL was increased after exposure to high glucose. The silencing of CD36 reduced the induction of CD36 and the expression of calcification enzymes and mineralization of VSMC. Our results indicate that CD36 signaling is partially involved in hyperglycemia and oxLDL-induced vascular calcification in diabetes.
Grants:	Instituto de Salud Carlos III CP15/00126 Instituto de Salud Carlos III PI17/01837 Instituto de Salud Carlos III PI14/1772 Instituto de Salud Carlos III PI18/00919 Instituto de Salud Carlos III CP15/00126
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	Scavenger receptor CD36 ; Atherosclerosis ; Diabetes ; Inflammation ; Vascular calcification
Published in:	International journal of molecular sciences, Vol. 21 (october 2020) , ISSN 1422-0067

DOI: 10.3390/ijms21197360
PMID: 33028031

19 p, 1.2 MB

The record appears in these collections:
Research literature > UAB research groups literature > Research Centres and Groups (research output) > Health sciences and biosciences > Institut d'Investigació en Ciencies de la Salut Germans Trias i Pujol (IGTP)
Research literature > UAB research groups literature > Research Centres and Groups (research output) > Health sciences and biosciences > Institut de Recerca Sant Pau
Articles > Research articles
Articles > Published articles