[논문]Nucleotide‐binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions

Kwon, Min‐; Young; Hwang, Narae; Back, Sung Hoon; Lee, Seon‐; Jin; Perrella, Mark A.; Chung, Su Wol

doi:10.1111/febs.15294

[해외논문] Nucleotide‐binding oligomerization domain protein 2 deficiency enhances CHOP expression and plaque necrosis in advanced atherosclerotic lesions 원문보기

The FEBS journal, v.287 no.10, 2020년, pp.2055 - 2069

Kwon, Min‐Young (Laboratory of Molecular Immunology, Department of Biological Sciences, University of Ulsan, South Korea) , Hwang, Narae (Laboratory of Molecular Immunology, Department of Biological Sciences, University of Ulsan, South Korea) , Back, Sung Hoon (Laboratory of Molecular Immunology, Department of Biological Sciences, University of Ulsan, South Korea) , Lee, Seon‐Jin (Environmental Disease Research Center, KRIBB, Daejeon, Korea) , Perrella, Mark A. (Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA) , Chung, Su Wol (Laboratory of Molecular Immunology, Department of Biological Sciences, University of Ulsan, South Korea)

Abstract ▼ AI-Helper

Endoplasmic reticulum (ER) stress‐induced cell death of vascular smooth muscle cells (VSMCs) is extensively involved in atherosclerotic plaque stabilization. We previously reported that nucleotide‐binding oligomerization domain protein 2 (NOD2) participated in vascular homeostasis and tissue injury. However, the role and underlying mechanisms of NOD2 remain unknown in ER stress‐induced cell death of VSMC during vascular diseases, including advanced atherosclerosis. Here, we report that NOD2 specifically interacted with ER stress sensor activating transcription factor 6 (ATF6) and suppressed the expression of proapoptotic transcription factor CHOP (C/EBP homologous protein) during ER stress. CHOP‐positive cells were increased in neointimal lesions after femoral artery injury in NOD2‐deficient mice. In particular, a NOD2 ligand, MDP, and overexpression of NOD2 decreased CHOP expression in wild‐type VSMCs. NOD2 interacted with an ER stress sensor molecule, ATF6, and acted as a negative regulator for ATF6 activation and its downstream target molecule, CHOP, that regulates ER stress‐induced apoptosis. Moreover, NOD2 deficiency promoted disruption of advanced atherosclerotic lesions and CHOP expression in NOD2−/−ApoE−/− mice. Our findings indicate an unsuspected critical role for NOD2 in ER stress‐induced cell death.

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