Origin of Cells That Contribute to Neointima Growth

Iwata, Hiroshi; Sata, Masataka

doi:10.1161/circulationaha.108.782961

Cited by 9 publications

(7 citation statements)

References 21 publications

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“…This increase was however not statistically significant, was confined to the lumen of immature collaterals that failed to undergo expansion (Figure 1A) and is likely due to the fact that while SM-α-actin is expressed predominantly by contractile smooth muscle it can be expressed by other cell types relevant to the process of collateral remodeling including synthetic VSMCs, macrophages and myeloid progenitor cells. 17 No change in SM-MHC or SM-α-actin expression was observed during the course of CCG in the NZ (Figure II, Supplement). Expression of non-muscle myosin (NMHC-B), a marker of synthetic VSMC phenotype, inversely correlated with SM-MHC expression in both rat phenotypes (Figure 1B).…”

Section: Resultsmentioning

confidence: 93%

MicroRNA-145 Restores Contractile Vascular Smooth Muscle Phenotype and Coronary Collateral Growth in the Metabolic Syndrome

Hutcheson

Terry

Chaplin

et al. 2013

ATVB

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Objective Transient, repetitive occlusion stimulates collateral growth (CCG) in normal animals. Vascular smooth muscle cells (VSMCs) switch to synthetic phenotype early in CCG then return to contractile phenotype. CCG is impaired in the metabolic syndrome. We determined whether impaired CCG was due to aberrant VSMC phenotypic modulation by miR-145-mediated mechanisms and if restoration of physiological miR-145 levels in metabolic syndrome (JCR rat) improved CCG. Approach/Results CCG was stimulated by transient, repetitive LAD occlusion and evaluated after 9 days by coronary blood flow measurements (microspheres). miR-145 was delivered to JCR VSMCs via adenoviral vector (miR-145-Adv). In JCR rats, miR-145 was decreased late in CCG (~2 fold day 6; ~4 fold day 9 vs. SD), which correlated with decreased expression of SM-specific contractile proteins (~5 fold day 6; ~10 fold day 9 vs. SD) indicative of VSMCs’ failure to return to the contractile phenotype late in CCG. miR-145 expression in JCR rats (miR-145-Adv) on days 6–9 of CCG completely restored VSMCs contractile phenotype and CCG (CZ/NZ flow ratio was 0.93±0.09 JCR+miR-145-Adv vs. 0.12±0.02 JCR vs. 0.87±0.02 SD). Conclusions Restoration of VSMC contractile phenotype through miR-145 delivery is a highly promising intervention for restoration of CCG in the metabolic syndrome.

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Section: Resultsmentioning

confidence: 93%

MicroRNA-145 Restores Contractile Vascular Smooth Muscle Phenotype and Coronary Collateral Growth in the Metabolic Syndrome

Hutcheson

Terry

Chaplin

et al. 2013

ATVB

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“…Recent studies suggest that bone marrow-derived vascular progenitor cells significantly contribute to vascular repair and remodelling [53][54][55][56][57][58][59][60][61] and that local RAAS exists in the bone marrow, which may play a crucial role in vascular inflammation. [62][63][64] Marumo et al showed that aldosterone inhibits the formation of bone marrow-derived endothelial progenitor cells, suggesting that MR blockade and/or co-treatment with antioxidants may enhance vascular regeneration.…”

Section: Potential New Targets For Mr Blockade To Reverse Vascular Inmentioning

confidence: 99%

Pre-clinical data on the role of mineralocorticoid receptor antagonists in reversing vascular inflammation

Yagi

Sata

2011

European Heart Journal Supplements

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Aldosterone plays an important role in regulating extracellularvolume, and is the downstream modulator of the renin-angiotensin-aldosterone system. In addition, aldosterone also causes increased oxidative stress and decreased nitric oxide bioavailability that results in vascular inflammation. Aldosterone therefore functions to promote cardiovascular damage and remodelling not only in a blood pressuredependent manner but also in a blood pressure-independent manner. Abundant experimental evidence from animal models has documented the mechanisms whereby aldosterone causes these effects as well as the benefits of mineralocorticoid receptor (MR) blockade to reduce vascular inflammation. The anti-inflammatory effects of MR antagonism seen in clinical trials suggest that MR blockade will be an important therapeutic approach in the future.

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“…Pioneering work suggested that these progenitors differentiate into mature and functional endothelial cells (ECs) and SMCs, respectively, in physiological and pathological settings [11,13]. However, their functional contributions to atherogenesis remain unclear [14][15][16][17]. The evidence also indicated that some intimal SMC may originate from circulating monocytes or their subset [14,18,19].…”

Section: Introductionmentioning

confidence: 99%

Dynamic Interplay Between Smooth Muscle Cells and Macrophages in Vascular Disease

Iwata¹,

Aikawa²

2015

Muscle Cell and Tissue

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Vascular smooth muscle cells (SMCs) and monocytes/macrophages represent major players in atherosclerotic vascular diseases. In addition to physiological and pathological roles of each cell type in atherosclerosis, dynamic interplay between SMCs and monocytes/macrophages may contribute to the pathogenesis of atherosclerosis more critically than previously understood. Activated macrophages accelerate proatherogenic functions of SMCs in vascular lesions. Activated SMCs promote additional accumulation of pro-inflammatory macrophages through expression of chemoattractants. More recent evidence suggests the interchangeability between SMC and monocyte/macrophage lineages. Future efforts to understand such dynamic interactions between SMCs and macrophages may provide novel insight into the pathogenesis of vascular disease and the development of new classes of medical solutions.

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Origin of Cells That Contribute to Neointima Growth

Cited by 9 publications

References 21 publications

MicroRNA-145 Restores Contractile Vascular Smooth Muscle Phenotype and Coronary Collateral Growth in the Metabolic Syndrome

MicroRNA-145 Restores Contractile Vascular Smooth Muscle Phenotype and Coronary Collateral Growth in the Metabolic Syndrome

Pre-clinical data on the role of mineralocorticoid receptor antagonists in reversing vascular inflammation

Dynamic Interplay Between Smooth Muscle Cells and Macrophages in Vascular Disease

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