title: The sdLDL Reduces MRC1 Expression Level and Secretion of Histamin e in Differentiated M2-macrophages from Patients with Coronary Artery Stenosis.
abstract: The macrophage polarization is proposed to be involved in initial events and remodeling of atherosclerosis plaques. Mannose receptor, C type 1 (MRC1) is a trans-membrane glycoprotein participating in phagocytosis and, is highly expressed in the M2 macrophages.
  
  
  
  The aim of this study was to investigate the effects of sdLDL (small dense LDL) on the MRC1 gene expression level and secretion of histamine in the differentiated M2 macrophages from monocytes of patients with coronary artery stenosis and healthy subjects.
  
  
  
  The monocytes were isolated from healthy subjects (< 5% stenosis) and patients (> 70% stenosis, SVD (Single Vessel Disease), 2VD (Two-Vessel Disease) and 3VD (Three-Vessel Disease)) by RosetteSep kit and, were differentiated into M2 macrophages by macrophage colonystimulating factor (M-CSF). The sdLDL particles were obtained by PEG-combined precipitation method. The MRC1 gene expression and histamine levels were measured by RT-qPCR and ELISA techniques, respectively.
  
  
  
  The MRC1 gene expression level was significantly increased in M2 macrophages of healthy subjects (P=0.05) while it reduced in SVD (P=0.05), 2VD (P=0.01) and 3VD (P=0.9) patients after treatment with sdLDL. The histamine value secreted from M2 macrophages (7-day) was higher (>3-fold, P=0.02) in patients as compared to healthy controls.
  
  
  
  The results showed that the sdLDL particles reduce the MRC1 gene expression levels in the differentiated M2 macrophages from patients with coronary artery disease. Furthermore, they had high inflammatory capacity for the secretion of histamine.
authors.affiliation: Biochemistry Department, University of Medical Sciences, Tehran. Iran.
authors.forename: Ameneh
authors.initials: A
authors.lastname: Yarnazari
authors.affiliation: Biochemistry Department, University of Medical Sciences, Tehran. Iran.
authors.forename: Parisa
authors.initials: P
authors.lastname: Hassanpour
authors.affiliation: Biochemistry Department, University of Medical Sciences, Tehran. Iran.
authors.forename: Syed Reza
authors.initials: SR
authors.lastname: Hosseini-Fard
authors.affiliation: Shahid Rajaee Hospital, University of Medical Sciences, Tehran. Iran.
authors.forename: Abdollah
authors.initials: A
authors.lastname: Amirfarhangi
authors.affiliation: Biochemistry Department, Cellular and Molecular Research Center, University of Medical Sciences, Tehran. Iran.
authors.forename: Mohammad
authors.initials: M
authors.lastname: Najafi
mesh_terms: D016764:Cell Polarity; D002478:Cells, Cultured; D023921:Coronary Stenosis / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D015536:Down-Regulation; D006632:Histamine / Q000276:immunology*; D006801:Humans; D008077:Lipoproteins, LDL / Q000276:immunology*; D008264:Macrophages / Q000166:cytology / Q000276:immunology* / Q000473:pathology; D008562:Membrane Glycoproteins; D010587:Phagocytosis; D011971:Receptors, Immunologic / Q000235:genetics* / Q000276:immunology
chemical_list: D008077:Lipoproteins, LDL; C573543:MRC1 protein, human; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; D006632:Histamine
keywords: Macrophage; atherosclerosis; coronary arteries; histamine; sdLDL; stenosis