Intracellular transports and atherogenesis

Mirоnоv, Alexander A.; Сесорова, И. С.; Dimov, Ivan; Карелина, Наталья Рафаиловна; Beznoussenko, Galina V.

doi:10.2741/4854

Cited by 17 publications

(49 citation statements)

References 32 publications

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“…VSMC migration was found to be enhanced in SHR, which is supported by the results of previous studies [38][39][40]. Though VSMC migration into already populated intima or even after cellular destruction is very slow [41], it contributes to hypertension-induced maladaptive vascular remodeling [42]. Moreover, enhanced VSMC migration contributes to the atherogenic mechanisms and has implications for the atherogenesis of hypertension [2,43].…”

Section: Discussionsupporting

confidence: 76%

miR-31-5p Promotes Oxidative Stress and Vascular Smooth Muscle Cell Migration in Spontaneously Hypertensive Rats via Inhibiting FNDC5 Expression

Zhou

Zheng

et al. 2021

Biomedicines

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Oxidative stress and the migration of vascular smooth muscle cells (VSMCs) are important for vascular remodeling in a variety of vascular diseases. miR-31-5p promotes cell migration in colorectal cancer cells but inhibits cell migration in renal cell carcinoma. However, whether miR-31-5p is involved in oxidative stress and VSMC migration remains unknown. This study shows the crucial roles of miR-31-5p in oxidative stress and VSMC migration, as well as underlying mechanisms. Experiments were carried out in primary VSMCs from aortic media of Wistar–Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), as well as the A7r5 cell line. Oxidative stress was assessed by NADPH oxidase (NOX) expression, NOX activity, and reactive oxygen species (ROS) production. Cell migration was evaluated with a Boyden chamber assay and a wound healing assay. The miR-31-5p mimic and inhibitor promoted and attenuated oxidative stress and cell migration in the VSMCs of SHR, respectively. A dual-luciferase reporter assay indicated that miR-31-5p targeted the 3’UTR domain of FNDC5. The miR-31-5p level was raised and FNDC5 expression was reduced in the VSMCs of SHR compared with those of WKY. The miR-31-5p mimic reduced FNDC5 expression in the A7r5 cells and the VSMCs of both WKY and SHR, while the miR-31-5p inhibitor only increased FNDC5 expression in the VSMCs of SHR. Exogenous FNDC5 attenuated not only the oxidative stress and VSMC migration in SHR but also the roles of the miR-31-5p mimic in inducing oxidative stress and VSMC migration. These results indicate that miR-31-5p promotes oxidative stress and VSMC migration in SHR via inhibiting FNDC5 expression. The increased miR-31-5p and reduced FNDC5 in the VSMCs of SHR contribute to enhanced oxidative stress and cell migration.

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Section: Discussionsupporting

confidence: 76%

miR-31-5p Promotes Oxidative Stress and Vascular Smooth Muscle Cell Migration in Spontaneously Hypertensive Rats via Inhibiting FNDC5 Expression

Zhou

Zheng

et al. 2021

Biomedicines

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“…Thus, only lipid transfer proteins can deliver cholesterol and free fatty acids from one membrane to another. Numerous (now more than 131) lipid- and sterol-transfer proteins have been identified to mediate directional cholesterol transfer at membrane contact sites formed between two closely apposed organelles (reviewed by Mironov et al [ 85 ]). However, it not known how lipids are moved from OMM to IMM.…”

Section: Membrane Geometry and Organelle Dynamicsmentioning

confidence: 99%

“…This process does not contradict the curvature hypothesis because insertion of caveolin and cavins into the lipid leaflet from the cytosol side increases the TAA and stimulates the PM invaginations into the cytosol. However, in an adipose tissue, caveolae and their derivate could be mostly important for temporal storage of fatty acids and cholesterol [ 85 ]. Thus, formation and disassembly of caveolae could be a dynamic process, and they consume the excess of the PM surface area after contraction of cells.…”

Section: Membrane Geometry and Organelle Dynamicsmentioning

confidence: 99%

Membrane Curvature, Trans-Membrane Area Asymmetry, Budding, Fission and Organelle Geometry

Mirоnоv

Mironov

Derganc

et al. 2020

IJMS

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In biology, the modern scientific fashion is to mostly study proteins. Much less attention is paid to lipids. However, lipids themselves are extremely important for the formation and functioning of cellular membrane organelles. Here, the role of the geometry of the lipid bilayer in regulation of organelle shape is analyzed. It is proposed that during rapid shape transition, the number of lipid heads and their size (i.e., due to the change in lipid head charge) inside lipid leaflets modulates the geometrical properties of organelles, in particular their membrane curvature. Insertion of proteins into a lipid bilayer and the shape of protein trans-membrane domains also affect the trans-membrane asymmetry between surface areas of luminal and cytosol leaflets of the membrane. In the cases where lipid molecules with a specific shape are not predominant, the shape of lipids (cylindrical, conical, or wedge-like) is less important for the regulation of membrane curvature, due to the flexibility of their acyl chains and their high ability to diffuse.

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“…A thrombus formed at the site of the eroded plaque contains leukocytes enriched with myeloperoxidase (MPO); neutrophils release proteolytic enzymes, MPO, together with DNA strings upon the formation of NETs [3]. However, there is little information on the contribution of lipoproteins to plaque erosion; and human arterial tissue is slightly different from that of athero-protective small animals [4], hence, this review focuses on the vulnerable plaques in human atherosclerosis.…”

Section: Introduction 1atherosclerotic Lesionmentioning

confidence: 99%

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

et al. 2021

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Oxidative modification of lipoproteins is implicated in the occurrence and development of atherosclerotic lesions. Earlier studies have elucidated on the mechanisms of foam cell formation and lipid accumulation in these lesions, which is mediated by scavenger receptor-mediated endocytosis of oxidized low-density lipoprotein (oxLDL). Mounting clinical evidence has supported the involvement of oxLDL in cardiovascular diseases. High-density lipoprotein (HDL) is known as anti-atherogenic; however, recent studies have shown circulating oxidized HDL (oxHDL) is related to cardiovascular diseases. A modified structure of oxLDL, which was increased in the plasma of patients with acute myocardial infarction, was characterized. It had two unique features: (1) a fraction of oxLDL accompanied oxHDL, and (2) apoA1 was heavily modified, while modification of apoB, and the accumulation of oxidized phosphatidylcholine (oxPC) and lysophosphatidylcholine (lysoPC) was less pronounced. When LDL and HDL were present at the same time, oxidized lipoproteins actively interacted with each other, and oxPC and lysoPC were transferred to another lipoprotein particle and enzymatically metabolized rapidly. This brief review provides a novel view on the dynamics of oxLDL and oxHDL in circulation.

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Intracellular transports and atherogenesis

Cited by 17 publications

References 32 publications

miR-31-5p Promotes Oxidative Stress and Vascular Smooth Muscle Cell Migration in Spontaneously Hypertensive Rats via Inhibiting FNDC5 Expression

miR-31-5p Promotes Oxidative Stress and Vascular Smooth Muscle Cell Migration in Spontaneously Hypertensive Rats via Inhibiting FNDC5 Expression

Membrane Curvature, Trans-Membrane Area Asymmetry, Budding, Fission and Organelle Geometry

Structure and Dynamics of Oxidized Lipoproteins In Vivo: Roles of High-Density Lipoprotein

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