Discipline of Biosciences and Biomedical Engineering (BSBE), Indian Institute of Technology Indore (IITI), Indore, Madhya Pradesh, India.
Discipline of Chemistry, Indian Institute of Technology Indore (IITI), Indore, Madhya Pradesh, India.
Cell Biol Int. 2021 Jun;45(6):1191-1201. doi: 10.1002/cbin.11558. Epub 2021 Feb 4.
Atherosclerosis is a chronic inflammatory disease arising due to an imbalance in lipid metabolism and maladaptive immune response driven by the accumulation of cholesterol-laden macrophages in the artery wall. Interactions between monocytes/macrophages and endothelial cells play an essential role in the pathogenesis of atherosclerosis. In our current study, nitric oxide synthase 1 (NOS1)-derived nitric oxide (NO) has been identified as a regulator of macrophage and endothelial cell interaction. Oxidized LDL (OxLDL) activates NOS1, which results in the expression of CD40 ligand in macrophages. OxLDL-stimulated macrophages produce some soluble factors which increase the CD40 receptor expression in endothelial cells. This increases the interaction between the macrophages and endothelial cells, which leads to an increase in the inflammatory response. Inhibition of NOS1-derived NO might serve as an effective strategy to reduce foam cell formation and limit the extent of atherosclerotic plaque expansion.
动脉粥样硬化是一种慢性炎症性疾病，由于脂质代谢失衡和胆固醇负荷巨噬细胞在动脉壁中的积累导致适应性免疫反应失调而引起。单核细胞/巨噬细胞与内皮细胞之间的相互作用在动脉粥样硬化的发病机制中起着至关重要的作用。在我们目前的研究中，一氧化氮合酶 1（NOS1）衍生的一氧化氮（NO）已被确定为调节巨噬细胞和内皮细胞相互作用的调节剂。氧化型低密度脂蛋白（OxLDL）激活 NOS1，导致巨噬细胞中 CD40 配体的表达。OxLDL 刺激的巨噬细胞产生一些可溶性因子，增加内皮细胞中 CD40 受体的表达。这增加了巨噬细胞和内皮细胞之间的相互作用，导致炎症反应增加。抑制 NOS1 衍生的 NO 可能是减少泡沫细胞形成和限制动脉粥样硬化斑块扩张程度的有效策略。
