Oxidative stress in vascular calcification

Hu, Chu-Ting; Shao, Yi-Duo; Liu, Yizhang; Xiao, Xuan; Cheng, Zhe-Bin; Qu, Shun-Lin; Huang, Liang

doi:10.1016/j.cca.2021.04.012

Cited by 48 publications

(29 citation statements)

References 149 publications

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“…As a consequence, macrophage-induced inflammation can reduce the production of VC inhibitors, such as fetuin-A ( Moe and Chen, 2005 ), a protein that can bind excess mineral and increase their plasma solubility ( Komaba and Fukagawa, 2009 ). Furthermore, an increase in reactive oxygen species (ROS) production is involved in VSMC osteochondrogenic trans-differentiation during the VC process ( Tóth et al, 2020 ; Hu et al, 2021 ). Recent studies have highlighted the role of extracellular vesicles (EVs) in VC ( Hodroge et al, 2017 ; Mansour et al, 2020 ; Yaker et al, 2020 ; Qin et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress

Yaker

Tebani

Lesueur

et al. 2022

Front. Cell Dev. Biol.

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Background: Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate among patients with diseases such as atherosclerosis and chronic kidney disease. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete a heterogeneous population of extracellular vesicles (EVs). Recent studies have shown involvement of EVs in the inflammation and oxidative stress observed in VC. We aimed to decipher the role and mechanism of action of macrophage-derived EVs in the propagation of inflammation and oxidative stress on VSMCs during VC.Methods: The macrophage murine cell line RAW 264.7 treated with lipopolysaccharide (LPS-EK) was used as a cellular model for inflammatory and oxidative stress. EVs secreted by these macrophages were collected by ultracentrifugation and characterized by transmission electron microscopy, cryo-electron microscopy, nanoparticle tracking analysis, and the analysis of acetylcholinesterase activity, as well as that of CD9 and CD81 protein expression by western blotting. These EVs were added to a murine VSMC cell line (MOVAS-1) under calcifying conditions (4 mM Pi—7 or 14 days) and calcification assessed by the o-cresolphthalein calcium assay. EV protein content was analyzed in a proteomic study and EV cytokine content assessed using an MSD multiplex immunoassay.Results: LPS-EK significantly decreased macrophage EV biogenesis. A 24-h treatment of VSMCs with these EVs induced both inflammatory and oxidative responses. LPS-EK-treated macrophage-derived EVs were enriched for pro-inflammatory cytokines and CAD, PAI-1, and Saa3 proteins, three molecules involved in inflammation, oxidative stress, and VC. Under calcifying conditions, these EVs significantly increase the calcification of VSMCs by increasing osteogenic markers and decreasing contractile marker expression.Conclusion: Our results show that EVs derived from LPS-EK–treated-macrophages are able to induce pro-inflammatory and pro-oxidative responses in surrounding cells, such as VSMCs, thus aggravating the VC process.

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Section: Introductionmentioning

confidence: 99%

Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress

Yaker

Tebani

Lesueur

et al. 2022

Front. Cell Dev. Biol.

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“…It has been reported that oxidative stress plays a central role in aggravating organ damage, including that of the heart, kidneys, bones, and aortas of diabetic and CKD model rats [ 51 , 52 , 53 , 54 ]. Excessive oxidative stress has emerged as an important mediator promoting VC through mechanisms such as VSMC differentiation, inflammation, DNA damage, and extracellular matrix remodeling [ 55 ]. Oxidative stress is associated with calcium deposition in blood vessel walls.…”

Section: Discussionmentioning

confidence: 99%

Potential Actions of Baicalein for Preventing Vascular Calcification of Smooth Muscle Cells In Vitro and In Vivo

Sulistyowati

Hsu

Lee

et al. 2022

IJMS

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Vascular calcification (VC) is associated with cardiovascular disease. Baicalein, a natural flavonoid extract of Scutellaria baicalensis rhizome has several biological properties which may inhibit VC. We investigated whether baicalein suppresses Runt-related transcription factor 2 (Runx2) and bone morphogenetic protein 2 (BMP-2) and upregulates smooth muscle 22-alpha (SM22-α) and alpha-smooth muscle actin (α-SMA). In an In Vitro experiment, primary rat aortic vascular smooth muscle cells (VSMCs) were pretreated with 0.1, 1, and 5 μM baicalein, followed by β-glycerophosphate (β-GP) to induce calcification. In an In Vivo experiment, VC was generated by vitamin D3 plus nicotine (VDN) administration to male Sprague Dawley (SD) rats randomly assigned into a control group, a VC group, a VC group pretreated with baicalein, and a baicalein alone group. Each group comprised 10 rats. Left ventricular (LV) morphology, function and performance were assessed by echocardiography. Calcium content was measured by Alizarin red S staining and alkaline phosphatase (ALP) activity assays. Apoptotic VSMCs were detected by flow cytometry. Protein levels and superoxide changes were evaluated using Western blotting and immunofluorescence assays respectively. Plasma malondialdehyde (MDA) was assayed. Baicalein pretreatment significantly reduced calcium content in calcified VSMCs (p < 0.001) as well as in VC rat aortic smooth muscle (p < 0.001). Additionally, ALP activity was decreased in calcified VSMCs and VC rat aortic smooth muscle (p < 0.001). Apoptosis was significantly attenuated by 1 μM baicalein pretreatment in calcified VSMCs. Runx2 and BMP-2 expressions were downregulated by the baicalein in calcified VSMCs. Baicalein pretreatment increased typical VSMCs markers SM22-α and α-SMA in calcified VSMCs. Baicalein pretreatment was associated with adverse changes in LV morphometry. Markers of oxidative stress declined, and endogenous antioxidants increased in VC rats pretreated with baicalein. Baicalein mitigates VC through the inhibition of Runx2/BMP-2 signaling pathways, enhancement of vascular contractile phenotype and oxidative stress reduction. However, our study is of basic experimental design; more advanced investigations to identify other molecular regulators of VC and their mechanisms of action is required.

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“…Emerging evidence suggests that autophagy directly protects against VC where endosomes, dysfunctional mitochondria, autophagic vesicles and Ca2+ and phosphate (Pi) enriched matrix laden EVs may work collectively to underpin the pathogenesis of VC. Excess ROS-induced stress has emerged as a critical mediator promoting VC through several mechanisms, including phosphate balance, phenotypic modulation of vSMCs, inflammation, DNA damage, and extracellular matrix remodelling ( Hu et al, 2021 ).…”

Section: Endothelial Exosomesmentioning

confidence: 99%

Exosomal Composition, Biogenesis and Profiling Using Point-of-Care Diagnostics—Implications for Cardiovascular Disease

Burtenshaw

Regan

Owen

et al. 2022

Front. Cell Dev. Biol.

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Arteriosclerosis is an important age-dependent disease that encompasses atherosclerosis, in-stent restenosis (ISR), pulmonary hypertension, autologous bypass grafting and transplant arteriosclerosis. Endothelial dysfunction and the proliferation of vascular smooth muscle cell (vSMC)-like cells is a critical event in the pathology of arteriosclerotic disease leading to intimal-medial thickening (IMT), lipid retention and vessel remodelling. An important aspect in guiding clinical decision-making is the detection of biomarkers of subclinical arteriosclerosis and early cardiovascular risk. Crucially, relevant biomarkers need to be good indicators of injury which change in their circulating concentrations or structure, signalling functional disturbances. Extracellular vesicles (EVs) are nanosized membraneous vesicles secreted by cells that contain numerous bioactive molecules and act as a means of intercellular communication between different cell populations to maintain tissue homeostasis, gene regulation in recipient cells and the adaptive response to stress. This review will focus on the emerging field of EV research in cardiovascular disease (CVD) and discuss how key EV signatures in liquid biopsies may act as early pathological indicators of adaptive lesion formation and arteriosclerotic disease progression. EV profiling has the potential to provide important clinical information to complement current cardiovascular diagnostic platforms that indicate or predict myocardial injury. Finally, the development of fitting devices to enable rapid and/or high-throughput exosomal analysis that require adapted processing procedures will be evaluated.

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Oxidative stress in vascular calcification

Cited by 48 publications

References 149 publications

Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress

Extracellular Vesicles From LPS-Treated Macrophages Aggravate Smooth Muscle Cell Calcification by Propagating Inflammation and Oxidative Stress

Potential Actions of Baicalein for Preventing Vascular Calcification of Smooth Muscle Cells In Vitro and In Vivo

Exosomal Composition, Biogenesis and Profiling Using Point-of-Care Diagnostics—Implications for Cardiovascular Disease

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