The Pathogenesis of Atherosclerosis: Atherogenesis and Inflammation

Munro, J M; Cotran, Ramzi S.

doi:10.1007/978-1-4612-4502-5_10

Cited by 306 publications

(248 citation statements)

References 105 publications

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“…6, E and F), and we suspect that they contribute to the increase in lipid content of plaques induced by PM 10 exposure. This is consistent with our previous finding (45) that the progression of atherosclerosis induced by PM 10 is characterized by plaques containing more lipids, a feature associated with plaque vulnerability and plaque rupture (31,38).…”

Section: Discussionsupporting

confidence: 94%

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Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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demiologic studies have shown an association between exposure to ambient particulate air pollution Ͻ10 m in diameter (PM10) and increased cardiovascular morbidity and mortality. We previously showed that PM10 exposure causes progression of atherosclerosis in coronary arteries. We postulate that the recruitment of monocytes from the circulation into atherosclerotic lesions is a key step in this PM10-induced acceleration of atherosclerosis. The study objective was to quantify the recruitment of circulating monocytes into vessel walls and the progression of atherosclerotic plaques induced by exposure to PM10. Female Watanabe heritable hyperlipidemic rabbits, which naturally develop systemic atherosclerosis, were exposed to PM10 (EHC-93) or vehicle by intratracheal instillation twice a week for 4 wk. Monocytes, labeled with 5-bromo-2Ј-deoxyuridine (BrdU) in donors, were transfused to recipient rabbits as whole blood, and the recruitment of BrdU-labeled cells into vessel walls and plaques in recipients was measured by quantitative histological methodology. Exposure to PM10 caused progression of atherosclerotic lesions in thoracic and abdominal aorta. It also decreased circulating monocyte counts, decreased circulating monocytes expressing high levels of CD31 (platelet endothelial cell adhesion molecule-1) and CD49d (very late antigen-4 ␣-chain), and increased expression of CD54 (ICAM-1) and CD106 (VCAM-1) in plaques. Exposure to PM10 increased the number of BrdU-labeled monocytes adherent to endothelium over plaques and increased the migration of BrdU-labeled monocytes into plaques and smooth muscle underneath plaques. We conclude that exposure to ambient air pollution particles promotes the recruitment of circulating monocytes into atherosclerotic plaques and speculate that this is a critically important step in the PM10-induced progression of atherosclerosis. atherosclerosis; adhesion molecules EPIDEMIOLOGIC STUDIES have associated exposure to ambient particulate air pollution Ͻ10 m in diameter (PM 10

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Section: Discussionsupporting

confidence: 94%

“…Atherosclerosis is an inflammatory disease of vessel walls in which monocytes play a pivotal role in its pathogenesis (31,38,47). Monocytes migrate into the vessel wall, where they differentiate into macrophages and express scavenger receptors that allow them to phagocytose modified lipoproteins.…”

mentioning

confidence: 99%

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Yatera

Hsieh²,

Hogg³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Then, monocyte/macrophage infiltration in the subendothelial space accompanied by serum lipid permeation and the migration of medial smooth muscle cells into the intima. 1 Macrophages and smooth muscle cells become foam cells as a result of lipid phagocytosis, and a fatty streak, a macroscopically identifiable intimal lesion, is formed in the affected intima. 2 Fatty streak can develop into advanced lesions, such as atheroma, and subsequently complicated lesions over several decades.…”

mentioning

confidence: 99%

“…2 Fatty streak can develop into advanced lesions, such as atheroma, and subsequently complicated lesions over several decades. 1,3,4 Various risk factors, such as hypertension, hypercholesterolemia, cigarette smoking, diabetes mellitus, genetic alterations, and familial predisposition affect the progression of atherosclerosis. 3,5 It is recognized that apoptosis takes place in atherosclerotic lesions, and that the rate of apoptosis varies (o2-30%).…”

mentioning

confidence: 99%

Role of macrophage and smooth muscle cell apoptosis in association with oxidized low-density lipoprotein in the atherosclerotic development

et al. 2005

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To examine the role of the apoptosis of macrophages and smooth muscle cells in the development of atherosclerosis, human aortic tissues with intimal lesions were immunostained with antibodies against terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL), single-stranded DNA (clone F7-26), and active caspase-3. Apoptotic cells were detected in the intima using both TUNEL and singlestranded DNA, however, the latter method was the more sensitive one for detecting apoptotic cells in the early stages of atherosclerosis. The number of apoptotic cells increased as the disease progressed. It implies that the apoptosis of intimal cells is involved in the formation of atherosclerotic lesions. In addition, quantitative analyses of the cell types undergoing apoptosis using double-immunostaining revealed that the susceptibility of macrophages and smooth muscle cells to apoptosis was greater specifically in atheroma than in the other atherosclerotic lesions, and macrophages were more susceptible to apoptosis than smooth muscle cells. The frequency and spatial distribution of oxidized low-density lipoprotein (oxLDL) (FOH1a/DLH3)-positive cells were examined by immunohistochemistry, and the results resembled those of apoptotic cells. The number of oxLDLpositive cells in the intima significantly correlated with the susceptibility of smooth muscle cells, but not with that of macrophages, to apoptosis. These results suggest that oxLDL affects the apoptosis of smooth muscle cells during the atherosclerotic development.

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“…1,2 Oxidized LDL, one of the factors thought to affect vessel wall integrity, 3 can lead to an inflammatory response. 4 Such a response will induce endothelial cell activation, extravasation of leukocytes, and migratory/reparative process by vascular smooth muscle. 5,6 Activated endothelium will express in sequence a series of adhesion molecules and powerful cofactors such as chemokines, which together will tether and activate leukocyte integrin complexes.…”

mentioning

confidence: 99%

ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE ⁻ ^/− /ICAM-1 ⁻ ^/− ) Fed a Fat or a Chow Diet

Bourdillon

Poston

Covacho

et al. 2000

ATVB

147

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Abstract-Intercellular adhesion molecule (ICAM)-1, a major adhesion molecule, plays a critical role in the homing of leukocytes to sites of atherosclerotic lesions. However, very little is known on the role of ICAM-1 in initiating and perpetuating vascular lesions in ApoE Ϫ/Ϫ mice fed a chow or a fat diet. This study has investigated the mean aortic lesions in mice (C57BL6 background) with a single-knockout (ApoE Ϫ/Ϫ ) or double-knockout (DKO; ApoE Ϫ/Ϫ , ICAM-1 Ϫ/Ϫ ) fed a chow or a fat diet over a period of 3, 6, 15, and 20 weeks. A 3-fold reduction in lesion size was observed at all time points in DKO mice fed a chow diet. However, in DKO mice fed a fat diet, a marked reduction in the aortic lesion was observed at 3 and 15 weeks, which did not reach a significant level at 6 and 20 weeks. This study shows in essence that DKO mice are protected from developing significant lesions for up to 6 weeks when fed a chow diet and from 3 to 6 weeks when fed a fat diet. After 6 weeks, the lesion size of the DKO mice follows that of the single-knockout mice when fed a chow diet and gets to the same level in mice fed a fat diet. Plasma cholesterol levels were not altered as a result of ICAM-1 deficiency. These studies show that ICAM-1 is implicated in the formation and progression of atherosclerotic lesions.

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The Pathogenesis of Atherosclerosis: Atherogenesis and Inflammation

Cited by 306 publications

References 105 publications

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Role of macrophage and smooth muscle cell apoptosis in association with oxidized low-density lipoprotein in the atherosclerotic development

ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE ⁻ ^/− /ICAM-1 ⁻ ^/− ) Fed a Fat or a Chow Diet

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The Pathogenesis of Atherosclerosis: Atherogenesis and Inflammation

Cited by 306 publications

References 105 publications

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Particulate matter air pollution exposure promotes recruitment of monocytes into atherosclerotic plaques

Role of macrophage and smooth muscle cell apoptosis in association with oxidized low-density lipoprotein in the atherosclerotic development

ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE − /− /ICAM-1 − /− ) Fed a Fat or a Chow Diet

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ICAM-1 Deficiency Reduces Atherosclerotic Lesions in Double-Knockout Mice (ApoE ⁻ ^/− /ICAM-1 ⁻ ^/− ) Fed a Fat or a Chow Diet