NOS1‐derived nitric oxide facilitates macrophage uptake of low‐density lipoprotein

Roy, Anjali; Banerjee, Sreeparna; Saqib, Uzma; Baig, Mirza S.

doi:10.1002/jcb.28439

Cited by 8 publications

(4 citation statements)

References 62 publications

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“…Transcriptionally regulated NOS2 (inducible NOS; NOS2) can produce large amounts of NO for prolonged periods of time while the activity-regulated constitutive isoforms NOS1 (neuronal NOS) and NOS3 (endothelial NOS) respond rapidly to calcium signals [26]. While the role of NOS2 in the anti-microbial activity of ΜΦs is well known [26], NOS1 is required for ΜΦ uptake of LDL during foam cell formation [27] and NOS3 may contribute to the initiation of the immune response [28]. In humans, special mention is required for the expression of NOS2 by activated pro-inflammatory ΜΦs.…”

Section: The Dual Role Of Macrophages During Inflammation and Resolutmentioning

confidence: 99%

Self-defense of macrophages against oxidative injury: Fighting for their own survival

et al. 2019

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Activated macrophages play a central role in both the development and resolution of inflammation. These immune cells need to be functional in harmful conditions with high levels of reactive oxygen and nitrogen species that can damage their basic cell components, which may alter their metabolism. An excessive accumulation of these cell alterations drives macrophages inexorably to cell death, which has been associated to the development of several inflammatory diseases and even with aging in a process termed as “immunosenescence”. Macrophages, however, exhibit a prolonged survival in this hostile environment because they equip themselves with a complex network of protective mechanisms. Here we provide an overview of these self-defense mechanisms with special attention being paid to bioactive lipid mediators, NRF2 signaling and metabolic reprogramming.

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Section: The Dual Role Of Macrophages During Inflammation and Resolutmentioning

confidence: 99%

Self-defense of macrophages against oxidative injury: Fighting for their own survival

et al. 2019

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“…In addition, NOS1 affects macrophage polarization toward the M1 state through the nuclear translocation and subunit assembly of activator protein 1 (AP1) [ 16 , 17 ]. Moreover, macrophage NOS1 modulates the inflammatory response and foam cell formation in atherosclerosis via the uptake of low-density lipoprotein (LDL) [ 18 , 19 ]. Thus, NOS1 participates in the regulation of macrophage polarization toward the M1 phenotype; however, whether NOS1 is involved in M2 macrophage polarization is not known.…”

Section: Introductionmentioning

confidence: 99%

Transcriptome profiling reveals new insights into the roles of neuronal nitric oxide synthase on macrophage polarization towards classically activated phenotype

et al. 2021

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In response to various stimuli, naïve macrophages usually polarize to M1 (classically activated) or M2 (alternatively activated) cells with distinct biological functions. Neuronal nitric oxide synthase (NOS1) is involved in M1 macrophage polarization at an early stage. Here, we show for the first time that NOS1 is dispensable for M2 macrophage polarization for the first time. Further, differentially expressed genes (DEGs) regulated by NOS1 signaling in M1-polarized macrophages stimulated with lipopolysaccharide (LPS) were characterized by transcriptome analysis of wild-type (WT) and NOS1 knockout mouse macrophages. Thousands of affected genes were detected 2 h post LPS challenge, and this wide-ranging effect became greater with a longer stimulation time (8 h post LPS). NOS1 deficiency caused dysregulated expression of hundreds of LPS-responsive genes. Most DEGs were enriched in biological processes related to transcription and regulation of the immune and inflammatory response. At 2 h post-LPS, the toll-like receptor (TLR) signaling pathway, cytokine–cytokine receptor interaction, and NOD-like receptor signaling pathway were the major pathways affected, whereas the main pathways affected at 8 h post-LPS were Th1 and Th2 cell differentiation, FoxO, and AMPK signaling pathway. Identified DEGs were validated by real-time quantitative PCR and interacted in a complicated signaling pathway network. Collectively, our data show that NOS1 is dispensable for M2 macrophage polarization and reveal novel insights in the role of NOS1 signaling at different stages of M1 macrophage polarization through distinct TLR4 plasma membrane-localized and endosome-internalized signaling pathways.

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“…: 88669; Thermo Fisher Scientific). Total protein lysate was separated on SDS‐PAGE as previously described (Roy et al, 2019). The separated protein was blotted onto a nitrocellulose membrane and blocked with 5% skimmed milk for 90 min at room temperature with gentle shaking.…”

Section: Methodsmentioning

confidence: 99%

NOS1‐mediated macrophage and endothelial cell interaction in the progression of atherosclerosis

Roy

Saqib

Baig

2021

Cell Biology International

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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.

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NOS1‐derived nitric oxide facilitates macrophage uptake of low‐density lipoprotein

Cited by 8 publications

References 62 publications

Self-defense of macrophages against oxidative injury: Fighting for their own survival

Self-defense of macrophages against oxidative injury: Fighting for their own survival

Transcriptome profiling reveals new insights into the roles of neuronal nitric oxide synthase on macrophage polarization towards classically activated phenotype

NOS1‐mediated macrophage and endothelial cell interaction in the progression of atherosclerosis

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