Role of the Scavenger Receptor CD36 in Accelerated Diabetic Atherosclerosis

Autor: Navas Madroñal, Miquel, Castelblanco, Esmeralda, Camacho, Mercedes, Consegal, Marta, Ramírez-Morros, Anna, Sarrias, Maria-Rosa, Perez, Paulina, Alonso, Núria, Galán, María, Mauricio Puente, Dídac, Universitat Autònoma de Barcelona
Rok vydání: 2020
Předmět:
0301 basic medicine
CD36 Antigens
Male
Vascular smooth muscle
CD36
030204 cardiovascular system & hematology
Muscle
Smooth
Vascular

lcsh:Chemistry
0302 clinical medicine
lcsh:QH301-705.5
Spectroscopy
Vascular calcification
Medial arterial calcification
Receptors
Scavenger

biology
diabetes
Chemistry
Diabetes
Calcinosis
General Medicine
Middle Aged
Flow Cytometry
Computer Science Applications
Lipoproteins
LDL

vascular calcification
cardiology
Female
lipids (amino acids
peptides
and proteins)

medicine.symptom
scavenger receptor CD36
medicine.medical_specialty
Myocytes
Smooth Muscle

Inflammation
Catalysis
Article
Inorganic Chemistry
Diabetes Complications
03 medical and health sciences
Diabetes mellitus
Internal medicine
Diabetes Mellitus
medicine
Humans
Physical and Theoretical Chemistry
Scavenger receptor
Molecular Biology
Aged
business.industry
Organic Chemistry
medicine.disease
Atherosclerosis
Scavenger receptor CD36
030104 developmental biology
Glucose
Endocrinology
lcsh:Biology (General)
lcsh:QD1-999
inflammation
Hyperglycemia
Unfolded protein response
biology.protein
atherosclerosis
business
Calcification
Lipoprotein
Zdroj: Dipòsit Digital de Documents de la UAB
Universitat Autònoma de Barcelona
International Journal of Molecular Sciences
Volume 21
Issue 19
International Journal of Molecular Sciences, Vol 21, Iss 7360, p 7360 (2020)
r-IGTP. Repositorio Institucional de Producción Científica del Instituto de Investigación Germans Trias i Pujol
instname
ISSN: 1422-0067
Popis: 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&prime
dioctadecyl-3,3,3&prime
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.
Databáze: OpenAIRE