Immune and Smooth Muscle Cells Interactions in Atherosclerosis: How to Target a Breaking Bad Dialogue?

Ramel, Damien; Gayral, Stéphanie; Sarthou, Marie-Kerguelen; Augé, Nathalie; Nègre‐Salvayre, Anne; Laffargue, Muriel

doi:10.3389/fphar.2019.01276

Cited by 32 publications

(25 citation statements)

References 103 publications

(123 reference statements)

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“…Atherosclerosis is caused by an excessive accumulation of oxidized low-density lipoproteins (ox-LDLs) in the vascular intima, which is followed by plaque formation ( Aquila et al, 2019 ; Provenzano et al, 2019 ; Ramel et al, 2019 ). Atherosclerosis is an independent risk factor for coronary stenosis ( Bernelli et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

Zheng¹,

Lu²

2020

Front. Cell Dev. Biol.

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Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction is an initial step toward atherosclerosis development. Mitochondria damage correlates with ox-LDL-induced endothelial injury through an undefined mechanism. We explored the role of optic atrophy 1 (Opa1)-related mitochondrial fusion and mitophagy in ox-LDL-treated endothelial cells, focusing on mitochondrial damage and cell apoptosis. Oxidized low-density lipoprotein treatment reduced endothelial cell viability by increasing apoptosis. Endothelial cell proliferation and migration were also impaired by ox-LDL. At the molecular level, mitochondrial dysfunction was induced by ox-LDL, as demonstrated by decreased mitochondrial membrane potential, increased mitochondrial reactive oxygen species production, augmented mitochondrial permeability transition pore openings, and elevated caspase-3/9 activity. Mitophagy and mitochondrial fusion were also impaired by ox-LDL. Opa1 overexpression reversed this effect by increasing endothelial cell viability and decreasing apoptosis. Interestingly, inhibition of mitophagy or mitochondrial fusion through transfection of siRNAs against Atg5 or Mfn2, respectively, abolished the protective effects of Opa1. Our results illustrate the role of Opa1-related mitochondrial fusion and mitophagy in sustaining endothelial cell viability and mitochondrial homeostasis under ox-LDL stress.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

Zheng¹,

Lu²

2020

Front. Cell Dev. Biol.

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“…The inflammatory reaction expands into that adventitia which may facilitate enhanced infiltration of M1 positive inflammatory macrophages to the adventitia observed in Figure 3A. The adventitial component of atherosclerosis has recently been appreciated in mouse models and human coronaries with atherosclerosis 49‐51 …”

Section: Discussionmentioning

confidence: 95%

High‐fat diet‐induced GAIT element‐mediated translational silencing of mRNAs encoding inflammatory proteins in macrophage protects against atherosclerosis

et al. 2020

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Previously, we identified a mechanism of inflammation control directed by ribosomal protein L13a and "GAIT" (Gamma Activated Inhibitor of Translation) elements in target mRNAs and showed that its elimination in myeloid cell-specific L13a knockout mice (L13a KO) increased atherosclerosis susceptibility and severity. Here, we investigated the mechanistic basis of this endogenous defense against atherosclerosis. We compared molecular and cellular aspects of atherosclerosis in high-fat diet (HFD)-fed L13a KO and intact (control) mice. HFD treatment of control mice induced release of L13a from 60S ribosome, formation of RNA-binding complex, and subsequent GAIT element-mediated translational silencing. Atherosclerotic plaques from HFD-treated KO mice showed increased infiltration of M1 type inflammatory macrophages. Macrophages from KO mice showed increased phagocytic activity and elevated expression of LDL receptor and pro-inflammatory mediators. NanoString analysis of the plaques from KO mice showed upregulation of a number of mRNAs encoding inflammatory proteins. Bioinformatics analysis suggests the presence of the potential GAIT elements in the 3′UTRs of several of these mRNAs. Macrophage induces L13a/GAIT-dependent translational silencing of inflammatory genes in response to HFD as an endogenous defense against atherosclerosis in ApoE −/− model. K E Y W O R D S atherosclerosis, GAIT, inflammation, L13a, translational control

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“…Cholesterol loading to VSMCs was observed to stimulate many proinflammatory genes and reduce the expression of VSMC marker genes [9]. These VSMC-derived macrophage-like cells are unlike typical immune cells: They have low phagocytic capacity but promote atherosclerosis pathogenesis by exacerbating vascular inflammation [10].…”

Section: Introductionmentioning

confidence: 99%

Platonin, a Cyanine Photosensitizing Dye, Ameliorates Inflammatory Responses in Vascular Smooth Muscle Cells by Modulating Inflammatory Transcription Factors

et al. 2021

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Inflammation of the arterial wall is critical to atherosclerosis pathogenesis. The switch of vascular smooth muscle cells (VSMCs) to macrophage-like cells is essential in the exacerbation of vascular inflammation. Platonin, a cyanine photosensitizing dye, exhibits protective effects in sepsis, trauma, and acute ischemic stroke through its anti-inflammatory capacity in macrophages. The present study investigated the effects and underlying mechanisms of platonin in inflammatory VSMCs. Pretreatment with platonin suppressed the expression of inducible nitric oxide synthetase and mature interleukin-1β but not that of monocyte chemoattractant protein-1 (MCP-1) in VSMCs stimulated by a combination of lipopolysaccharide and interferon-γ (LPS/IFN-γ). Furthermore, platonin inhibited LPS/IFN-γ-induced Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation though the direct reduction of p65Ser536 phosphorylation but not the restoration of Inhibitor of nuclear factor kappa B (IκBα) degradation in VSMCs. However, platonin inhibited Oxidized low-density lipoprotein (ox-LDL)-induced MCP-1 production, possibly through the attenuation of Activator protein 1 (AP-1) binding activity and C-Jun N-terminal kinases ½ (JNK1/2) phosphorylation. Platonin also lowered lipid drop accumulation in VSMCs in Oil red O staining assay. The results collectively indicated that platonin has a vascular protective property with potent anti-inflammatory effects in VSMCs. In conclusion, platonin should be a potential for treating vascular inflammatory diseases such as atherosclerosis.

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Immune and Smooth Muscle Cells Interactions in Atherosclerosis: How to Target a Breaking Bad Dialogue?

Cited by 32 publications

References 103 publications

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

RETRACTED: Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy

High‐fat diet‐induced GAIT element‐mediated translational silencing of mRNAs encoding inflammatory proteins in macrophage protects against atherosclerosis

Platonin, a Cyanine Photosensitizing Dye, Ameliorates Inflammatory Responses in Vascular Smooth Muscle Cells by Modulating Inflammatory Transcription Factors

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