Atherosclerosis

1971

DOI: 10.1016/0021-9150(71)90003-7

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Cell proliferation in the atherosclerotic plaques of cholesterol-fed rabbits

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1972

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Cited by 44 publications

(10 citation statements)

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“…Once the lesion has formed, the highest apoptosis rates are found around the plaque stenosis (43) and can reach up to 50 times the baseline. Several studies of cell proliferation in plaques have reported increased mitosis of smooth muscle cells as well as other cells of undetermined type in the intima but not of the luminal ECs covering the plaque (10). In addition, most mediators of the inflammatory process associated with plaque formation (e.g., TNF-␣ and oxLDL) have been shown to increase EC apoptosis (15,20,24,36).…”

Section: Discussionmentioning

confidence: 99%

The role of mitosis in LDL transport through cultured endothelial cell monolayers

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²

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Cancel LM, Tarbell JM. The role of mitosis in LDL transport through cultured endothelial cell monolayers. Am J Physiol Heart Circ Physiol 300: H769 -H776, 2011. First published December 17, 2010 doi:10.1152 doi:10. /ajpheart.00445.2010 have previously shown that leaky junctions associated with dying or dividing cells are the dominant pathway for LDL transport under convective conditions, accounting for Ͼ90% of the transport. We (8) have also recently shown that the permeability of bovine aortic endothelial cell monolayers is highly correlated with their rate of apoptosis and that inhibiting apoptosis lowers the permeability of the monolayers to LDL. To explore the role of mitosis in the leaky junction pathway, the microtubule-stabilizing agent paclitaxel was used to alter the rate of mitosis, and LDL flux and water flux (Jv) were measured. Control monolayers had an average mitosis rate of 0.029%. Treatment with paclitaxel (2.5 M) for 1.5, 3, 4.5, or 6 h yielded increasing rates of mitosis ranging from 0.099% to 1.03%. The convective permeability of LDL (P e) increased up to fivefold, whereas Jv increased up to threefold, over this range of mitosis rates. We found strong correlations between the mitosis rate and both P e and Jv. However, compared with our previous apoptosis study (8), we found that mitosis was only half as effective as apoptosis in increasing P e. The results led us to conclude that while mitotsis-related leaky junctions might play a role in the initial infiltration of LDL into the artery wall, the progression of atherosclerosis might be more closely correlated with apoptosisrelated leaky junctions.low-density lipoprotein permeability; bovine aortic endothelial cells; water flux; leaky junctions; mitosis THE FIRST EVENT in the cascade of processes leading to atherosclerotic lesion formation is lipid infiltration and accumulation within the arterial wall (41). A relationship between enhanced endothelial permeability to LDL and the localization of atherosclerotic plaques is well established (16, 33). There are three potential pathways for the transport of macromolecules across the endothelium: transcytosis in vesicles, paracellular transport through breaks in the tight junction strand, and the leaky junction pathway associated with cells undergoing mitosis or apoptosis. Previous in vivo (13, 28, 29) and theoretical (48) studies have supported the importance of the leaky junction pathway in LDL and albumin transport across the endothelium. In studies by Lin et al. (30) and Chien et al. (13), aortic sections were stained with hematoxylin to identify cells in the M phase of the cell cycle using morphological criteria. Roughly 1 in 3,000 cells was found to be mitotic, but nearly all of those had an Evans blue-albumin (EBA) or Lucifer yellow (LY)-LDL leakage spot associated with it (99% for EBA and 80% for LY-LDL). Mitotic cells accounted for 30% of all EBA leaks and 45% of all LY-LDL leaks.Observations that hemodynamic factors usually associated with the development of atherosclerosis also affect end...

“…Once the lesion has formed, the highest apoptosis rates are found around the plaque stenosis (43) and can reach up to 50 times the baseline. Several studies of cell proliferation in plaques have reported increased mitosis of smooth muscle cells as well as other cells of undetermined type in the intima but not of the luminal ECs covering the plaque (10). In addition, most mediators of the inflammatory process associated with plaque formation (e.g., TNF-␣ and oxLDL) have been shown to increase EC apoptosis (15,20,24,36).…”

Section: Discussionmentioning

confidence: 99%

The role of mitosis in LDL transport through cultured endothelial cell monolayers

¹

,

²

2011

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Cancel LM, Tarbell JM. The role of mitosis in LDL transport through cultured endothelial cell monolayers. Am J Physiol Heart Circ Physiol 300: H769 -H776, 2011. First published December 17, 2010 doi:10.1152 doi:10. /ajpheart.00445.2010 have previously shown that leaky junctions associated with dying or dividing cells are the dominant pathway for LDL transport under convective conditions, accounting for Ͼ90% of the transport. We (8) have also recently shown that the permeability of bovine aortic endothelial cell monolayers is highly correlated with their rate of apoptosis and that inhibiting apoptosis lowers the permeability of the monolayers to LDL. To explore the role of mitosis in the leaky junction pathway, the microtubule-stabilizing agent paclitaxel was used to alter the rate of mitosis, and LDL flux and water flux (Jv) were measured. Control monolayers had an average mitosis rate of 0.029%. Treatment with paclitaxel (2.5 M) for 1.5, 3, 4.5, or 6 h yielded increasing rates of mitosis ranging from 0.099% to 1.03%. The convective permeability of LDL (P e) increased up to fivefold, whereas Jv increased up to threefold, over this range of mitosis rates. We found strong correlations between the mitosis rate and both P e and Jv. However, compared with our previous apoptosis study (8), we found that mitosis was only half as effective as apoptosis in increasing P e. The results led us to conclude that while mitotsis-related leaky junctions might play a role in the initial infiltration of LDL into the artery wall, the progression of atherosclerosis might be more closely correlated with apoptosisrelated leaky junctions.low-density lipoprotein permeability; bovine aortic endothelial cells; water flux; leaky junctions; mitosis THE FIRST EVENT in the cascade of processes leading to atherosclerotic lesion formation is lipid infiltration and accumulation within the arterial wall (41). A relationship between enhanced endothelial permeability to LDL and the localization of atherosclerotic plaques is well established (16, 33). There are three potential pathways for the transport of macromolecules across the endothelium: transcytosis in vesicles, paracellular transport through breaks in the tight junction strand, and the leaky junction pathway associated with cells undergoing mitosis or apoptosis. Previous in vivo (13, 28, 29) and theoretical (48) studies have supported the importance of the leaky junction pathway in LDL and albumin transport across the endothelium. In studies by Lin et al. (30) and Chien et al. (13), aortic sections were stained with hematoxylin to identify cells in the M phase of the cell cycle using morphological criteria. Roughly 1 in 3,000 cells was found to be mitotic, but nearly all of those had an Evans blue-albumin (EBA) or Lucifer yellow (LY)-LDL leakage spot associated with it (99% for EBA and 80% for LY-LDL). Mitotic cells accounted for 30% of all EBA leaks and 45% of all LY-LDL leaks.Observations that hemodynamic factors usually associated with the development of atherosclerosis also affect end...

“…This fact is also confirmed by C avallero el al. [3] who used tritiated thymidine. Monocytes are also present as has been described by R ada r el al.…”

Section: Discussionmentioning

confidence: 99%

Aortic Lathyrism: Ultrastructural Study of Lesions in the Aortic Wall and the Protective Effect of Pyridinol Carbamate

1974

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Electron-microscopic examination of aortas of rat treated orally and chronically with β-aminopropionitrile (BAPN) has shown progressive lesions in the elastic framework. This is associated with modifications of cells in the media which dedifferentiate into histiocytes and fibrocytes and also multiply. These changes begin in the 5th week of treatment, and are responsible for the hyperplasia of the intima as well as its thickening and collagenization. They support observations made in man during aortic aging, namely with regard to the intima and the intima-media junction. A high lipid diet given at various times during intoxication causes lipid deposition in the intima and a substantial penetration into the media when the lesions are developing. This also corroborates some hypotheses on the development of human atheroma. The addition of pyridinol carbamate (PDC) to BAPN prevents the formation of elastic tissue lesions. When given after the cessation of lathyrism treatment, PDC arrests and causes regression of lesions in the aortic media. It has no effects on lipid deposits, but the deposits are confined to the intima only.

“…As for the in situ proliferation of foam cells, several studies have been done, but none used any reliable markers to discriminate among the types of foam cells. [34][35][36][37][38] Recently in a study of Watanabe heritable hyperlipidemic and hypercholesterolemic fat-fed rabbits, Rosenfeld and Ross reported that proliferating macrophage-derived foam cells constituted up to 4% of the [3H]thymidine-labeled cells in the aorta of both kinds of rabbits, while the percentage of proliferating smooth muscle cell-derived foam cells was slightly higher, about 5%.-In the present study, the percentage of PCNApositive reaction or the labeling rate of [3H]thymidine in macrophage-derived or smooth muscle cell-derived foam cells in the atherosclerotic lesions of pulmonary arteries were below 3% at 60 and 90 days of cholesterol feeding. Based on all these data, we consider that during pulmonary atherogenesis small populations of macrophage or smooth muscle cell-derived foam cells in the wall of pulmonary arteries have the capacity to proliferate in situ.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical detection of macrophage‐derived foam cells and macrophage colony‐stimulating factor in pulmonary atherogenesis of cholesterol‐fed rabbits

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1995

Pathology International

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In order to investigate the role of monocyte/macrophages and their relationship to the expression of macrophage colony-stimulating factor (MCSF) in pulmonary atherosclerosis, lungs were excised from rabbits that had been fed for 60 and 90 days on a diet containing 0.5% cholesterol. In the lungs, fatty streaks and elevated foam cell lesions predominated in the large or medium-sized elastic pulmonary arteries, while massive accumulation of foam cells in the intima of muscular arteries produced marked luminal narrowing and nearly complete occlusion. In these lesions, most of the foam cells were reactive with RbM2, a monoclonal antibody (mAb) against rabbit macrophages, while smooth muscle cell-derived foam cells were detected by mAb against smooth muscle actin in the deeper area of elevated foam cell lesions of elastic arteries. Ultrastructural observation confirmed the presence of monocytes in the intima, their differentiation into macrophages, and their transformation into foam cells in the atherosclerotic lesions. Immunohistochemical expression of MCSF was demonstrated in the endothelial cells, smooth muscle cells and foam cells. A minor macrophage-derived foam cell population was demonstrated to possess a proliferative capacity. These data suggest that MCSF is involved in the differentiation of monocytes into macrophages, their transformation into foam cells, and their proliferation during pulmonary atherogenesis.

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