Vascular Function

Shimokawa, Hiroaki; Satoh, Kimio

doi:10.1161/atvbaha.114.304119

Cited by 28 publications

(9 citation statements)

References 33 publications

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“…ICAM-1 and VCAM-1 secreted by endothelial cells can promote the adhesion of monocytes to endothelial cells, increasing the chance of monocyte exudation. As monocytes play a direct role in the development of AS, it is reasonable to consider endothelial cell injury as a key component in the development of AS [26,27]. Based on the above findings, we generated an in vitro ox-LDL injury model of cultured vascular endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of a novel regulatory pathway for PPARα by RNA-seq characterization of the endothelial cell lipid peroxidative injury transcriptome

Dou

Liang

et al. 2019

Open Biol.

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Endothelial dysfunction caused by endothelial cell injuries is the initiating factor for atherosclerosis (AS), and lipid peroxidative injury is one of a dominant factor for AS pathogenesis. Using RNA-seq, we compared changes in transcriptome expression before and after endothelial cell injury, and found 311 differentially expressed genes (DEGs), of which 258 genes were upregulated and 53 genes were downregulated. The protein–protein interactions (PPIs) between the genes were analysed using the STRING database, and a PPI network of DEGs was constructed. The relationship distributions among these PPIs were analysed by performing network node statistics. We found that in the top 20 DEGs with high connected protein nodes in the PPI network, 16 were upregulated and 4 were downregulated. Gene ontology (GO) functional enrichment analysis and KEGG pathway enrichment analysis on the DEGs were also performed. By comparing the upregulated expressed genes with high connected protein nodes in the PPI network to those related to endothelial cell lipid damage and repair in the GO analysis, we identified seven genes (NOX4, PPARA, CCL2, PDGFB, IL8, VWF, CD36) and verified their expression levels by real-time polymerase chain reaction. The protein interactions between the seven genes were then analysed using the STRING database. The results predicted that CCL2 interacts with NOX4, PPARα, PDGFβ and VWF individually. Thus, we examined the protein expression levels of CCL2, NOX4, PPARα, PDGFβ and VWF, and found that the expression levels of all proteins were significantly upregulated after the lipid peroxidative injury, with CCL2 and PPARα exhibiting the highest expression levels. Therefore, we investigated the interregulatory relationship between CCL2 and PPARα and their roles in the repair of endothelial cell injury. With the help of gene overexpression and knockdown techniques, we discovered that PPARα promotes the repair of endothelial cell injury by upregulating CCL2 expression in human umbilical vein endothelial cells but that CCL2 cannot regulate PPARα expression. Therefore, we believe that PPARα participates in the repair of endothelial cell lipid peroxidative injury through regulating the expression of CCL2.

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Section: Discussionmentioning

confidence: 99%

Identification of a novel regulatory pathway for PPARα by RNA-seq characterization of the endothelial cell lipid peroxidative injury transcriptome

Dou

Liang

et al. 2019

Open Biol.

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“…A 250 μm cylinder with an inner diameter of 150 μm emulated the artery, which was positioned in the region between the cantilever and the bulk. Mechanical properties of this structure were defined according to bibliography to resemble those of microvessels (Izzard et al, 2005; Shimokawa and Satoh, 2014). Increasing mechanical loads were applied inside the artery simulating an increase of intraluminal pressure from 0 to 120 mmHg, which was in accordance to experimental myography assays with arterial segments (Rodríguez-Rodríguez et al, 2009; Ogalla et al, 2015).…”

Section: Resultsmentioning

confidence: 99%

Ultrasensitive Photonic Microsystem Enabling Sub-micrometric Monitoring of Arterial Oscillations for Advanced Cardiovascular Studies

et al. 2019

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Cardiovascular diseases are the first cause of death globally. Their early diagnosis requires ultrasensitive tools enabling the detection of minor structural and functional alterations in small arteries. Such analyses have been traditionally performed with video imaging-based myographs, which helped to investigate the pathophysiology of the microvessels. Since new vascular questions have emerged, substantial modifications are necessary to improve the performance of imaging and tracking software, reducing the cost and minimizing the microvessel cleaning and manipulation. To address these limitations, we present a photonic microsystem fabricated in polydimethylsiloxane and integrating micro-optical elements and a lightguide-cantilever for sub-micrometric analysis of small arteries (between 125 and 400 μm of basal diameter). This technology enables simultaneous measurement of arterial distension, stiffness, vasomotion, and heartbeat and without the need for advanced imaging system. The microsystem has a limit of detection of 2 μm, five times lower than video imaging-based myographs, is two times more sensitive than them (0.5 μm/mmHg), reduces variability to half and doubles the linear range reported in these myographs. More importantly, it allows the analysis of intact arteries preserving the integrity and function of surrounding tissues. Assays can be conducted in three configurations according to the surrounding tissue: (i) isolated arteries ( in vitro ) where the surrounding tissue is partially removed, (ii) non-isolated arteries ( in vivo ) with surrounding tissue partially removed, and (iii) intact arteries in vivo preserving surrounding tissue as well as function and integrity. This technology represents a step forward in the prediction of cardiovascular risk.

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“…39,40 Proinflammatory mediators (eg, monocyte chemotactic protein-1, interleukin-8, tumor necrosis factor, reactive oxygen species, and interleukin-1) along with the activation of endothelial cells by selectins arrange the capture, rolling, and activation of monocytes to undergo firm adhesion to endothelial cells, likely as reported in native disease. 41,42 It is also conceivable that macrophage proliferation may be involved, similar to native disease. 43 Continued inhibition of VSMC growth and persistent disruption of laminar flow with the addition of drug together with polymer-associated chronic inflammation all likely represent contributing factors to the acceleration neoatherosclerosis occurring within stents.…”

Section: E48 Arterioscler Thromb Vasc Biolmentioning

confidence: 99%

Neoatherosclerosis From a Pathologist’s Point of View

Romero

Yahagi

Kolodgie

et al. 2015

ATVB

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Figure 2. Progression of neoatherosclerosis occurring within drug-eluting stent (DES).A and B, Low-and high-power images of early atherosclerotic change characterized by luminal foam cells (arrows) with underlying fibrointimal thickening. C and D, Low-and high-power images of foamy macrophage clusters (arrows) in the peristrut region adjacent to luminal surface. E and F, Low-and high-power images of fibroatheroma with necrotic core (NC) within neointima. G and H, Low-and high-power images of thin cap fibroatheroma (arrows) with NC. I and J, Low-and high-power images of plaque rupture resulting in continuity between the overlying thrombus (Th) and the NC. * represents stent strut. Images E, F, and I are reprinted from Yahagi et al 1 with permission of the publisher.by guest on

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Vascular Function

Cited by 28 publications

References 33 publications

Identification of a novel regulatory pathway for PPARα by RNA-seq characterization of the endothelial cell lipid peroxidative injury transcriptome

Identification of a novel regulatory pathway for PPARα by RNA-seq characterization of the endothelial cell lipid peroxidative injury transcriptome

Ultrasensitive Photonic Microsystem Enabling Sub-micrometric Monitoring of Arterial Oscillations for Advanced Cardiovascular Studies

Neoatherosclerosis From a Pathologist’s Point of View

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