CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells

• Published in: Molecular and cellular biochemistry Vol. 463; no. 1-2; pp. 211 - 223
• Main Authors: Zahid, MD Khurshidul, Rogowski, Michael, Ponce, Christopher, Choudhury, Mahua, Moustaid-Moussa, Naima, Rahman, Shaikh M.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.01.2020; Springer; Springer Nature B.V
• Subjects: Animals; Apoptosis; Arteriosclerosis; Atherogenesis; Atherosclerosis; Autophagy; Biochemistry; Biomedical and Life Sciences; Cardiology; Caspase-1; CCAAT-Enhancer-Binding Protein-beta - genetics; CCAAT-Enhancer-Binding Protein-beta - metabolism; CCAAT/enhancer-binding protein; Cholesterol; Deactivation; Deregulation; Efflux; Endoplasmic reticulum; Endoplasmic Reticulum Stress; Foam Cells - metabolism; Foam Cells - pathology; Gene expression; Gene Expression Regulation; Gene Knockdown Techniques; Genes; Inactivation; Inflammation; Inflammation - genetics; Inflammation - metabolism; Inflammation - pathology; Kinases; Life Sciences; Lipid metabolism; Lipids; Lipoproteins, LDL - genetics; Lipoproteins, LDL - metabolism; Macrophages; Medical Biochemistry; Mice; NF-κB protein; Oncology; Phagocytosis; Phosphorylation; Protein binding; Proteins; Rapamycin; RAW 264.7 Cells; siRNA; Stress; TOR protein; Tumor necrosis factor-α; Type 2 diabetes; C/EBPβ; Autophagy; Macrophage foam cells; Endoplasmic reticulum stress (ERS); Apoptosis

Atherosclerosis is associated with deregulated cholesterol metabolism and formation of macrophage foam cells. CCAAT/enhancer-binding protein beta (C/EBPβ) is a transcription factor, and its inhibition has recently been shown to prevent atherosclerosis development and foam cell formation. However, wh...