Detection of Vascular Dendritic Cells and Extracellular Calcium-Binding Protein S-100 in Foci of Calcification in Human Arteries.

Bobryshev, Yuri V.; Lord, Reginald S. A.

doi:10.1267/ahc.28.371

Cited by 20 publications

(6 citation statements)

References 37 publications

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“…It is thought that destruction of these cells may be involved in the calcification process through release of the calcium binding protein S-100. 33 In agreement with our data, Hieshima et al 16 found that PARC mRNA could be induced in monocytes differentiated with LPS and in U937 cells stimulated with PMA. Also, in situ studies in lung sections showed high PARC expression in a subset of alveolar macrophages that stained positive for EBM11/CD68.…”

Section: Discussionsupporting

confidence: 93%

“…The presence of CD1a ϩ dendritic cells in atherosclerotic plaques has been reported in the literature. 32,33 However, it has not yet been clarified as to whether these cells play a role in antigen presentation during atherosclerosis. It is thought that destruction of these cells may be involved in the calcification process through release of the calcium binding protein S-100.…”

Section: Discussionmentioning

confidence: 99%

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Expression and Cellular Localization of the CC Chemokines PARC and ELC in Human Atherosclerotic Plaques

Reape

Rayner

Manning

et al. 1999

The American Journal of Pathology

101

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Local immune responses are thought to play an important role in the development of atherosclerosis. Histological studies have shown that human atherosclerotic lesions contain T lymphocytes throughout all stages of development, many of which are in an activated state. A number of novel CC chemokines have been described recently, which are potent chemoattractants for lymphocytes: PARC (pulmonary and activation-regulated chemokine), ELC (EBI1-ligand chemokine), LARC (liver and activation-regulated chemokine), and SLC (secondary lymphoid-tissue chemokine). Using reverse transcriptase-polymerase chain reaction and in situ hybridization, we have found gene expression for PARC and ELC but not for LARC or SLC in human atherosclerotic plaques. Immunohistochemical staining of serial plaque sections with specific cell markers revealed highly different expression patterns of PARC and ELC. PARC mRNA was restricted to CD68+ macrophages (n = 14 of 18), whereas ELC mRNA was widely expressed by macrophages and intimal smooth muscle cells (SMC) in nearly all of the lesions examined (n = 12 of 14). ELC mRNA was also found to be expressed in the medial SMC wall of highly calcified plaques (n = 4). Very low levels of ELC mRNA expression could also be detected in normal mammary arteries but no mRNA expression for PARC was detected in these vessels (n = 4). In vitro, ELC mRNA was found to be up-regulated in aortic SMC stimulated with tumor necrosis factor-a and interferon-gamma but not in SMC stimulated with serum. Both PARC and ELC mRNA were expressed by monocyte-derived macrophages but not monocytes. The expression patterns of PARC and ELC mRNA in human atherosclerotic lesions suggest a potential role for these two recently described CC chemokines in attracting T lymphocytes into atherosclerotic lesions.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Expression and Cellular Localization of the CC Chemokines PARC and ELC in Human Atherosclerotic Plaques

Reape

Rayner

Manning

et al. 1999

The American Journal of Pathology

101

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“…These include the calcifying vascular cells, described from in vitro studies as microvascular 'pericyte-like', 7,9 and vascular dendritic cells which produce the calcium-binding S-100 protein. 30 Moreover, vascular SMCs and macrophage-derived foam cells were recently shown to express the two bone-associated proteins osteopontin and matrix Gla protein, especially in association with necrotic lipid cores and areas of calcification. 24 However, the in vivo distributions and potential interactions of these 'calcifying' cells relative to macrophages, mast cells, and calcification sites remain uncertain.…”

Section: Discussionmentioning

confidence: 99%

Calcification in atherosclerotic plaque of human carotid arteries: associations with mast cells and macrophages

1998

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“…These observations suggest that elastocalcinosis involves both elastic fiber fragmentation and a loss of elastin cross-linking. A factor involved in osteogenetic vascular calcification, S-100 calciumbinding protein (10,11), is found in the medial calcium deposits (88,89).…”

Section: Potential Physiological Consequences Of Elastocalcinosismentioning

confidence: 99%

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Atkinson¹

2008

Journal of Applied Physiology

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Atkinson J. Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences. J Appl Physiol 105: 1643-1651, 2008. First published September 4, 2008 doi:10.1152/japplphysiol.90476.2008.-With age, the calcium content of the arterial wall increases. Calcification occurs at two main levels: intimal plaques and the medial elastic fiber network. The latter has been referred to as medial elastocalcinosis and is the subject of this review. The mechanisms involved in elastocalcinosis are complex and involve polar, apolar, and active processes. Vascular calcification may be species specific to humans. As laboratory animals, such as the rat, grow old, they suffer from only very mild arterial calcification. Different animal models of induction of massive arterial calcification by pharmacological and other means exist. Although extrapolation from such models to the clinical situation in terms of etiology is difficult, such models could be useful in the nonclinical study of the pathophysiological consequences of vascular calcification. Vascular calcification modifies arterial wall stiffness, and this could have clinically significant consequences on cardiac function and downstream circulatory control.artery; calcium; wall stiffness; aging Development of the Concept of ElastocalcinosisSeveral recent reviews deal with the subject of elastocalcinosis (1,21,25,41,54,56,82,108).Age-linked vascular calcification has been known since the nineteenth century (85,122). It appears to be "specific" in that vascular wall calcium and phosphorus contents increase with age, whereas there are no significant increases in the aortic content of most other elements, such as sodium, potassium, and magnesium (128). Vascular calcification linked to age is also specific for arteries and does not involve other soft tissues, such as veins (57,60,117). Vascular calcification is associated with hypertension. Blumenthal et al. (9) showed that the onset of arterial calcification occurs at an earlier age in hypertensive subjects. The association in humans between arterial calcification and hypertension has since been reported by many investigators (75). The etiology of the complex multifactorial interactions, however, between hypertension (and associated changes in vascular wall mechanics) and amplification of calcification remains obscure.Vascular calcification can occur in localized intimal plaques and in a diffuse fashion in the media (53), and often there is no indication in published reports of where samples were taken. Méndez and Tejada (76) reported that the calcium content of plaques is 10-fold higher than that of "plaque-free" artery. Thus "contamination" of samples with plaque material could mask medial, diffuse elastocalcinosis. It is to be noted that the calcium content of "normal" intima (i.e., free of plaques and fatty streaks) is low and shows only a slight increase with age (6, 29). Medial elastocalcinosis independent of atheroma-associated calcification has been demonstrated by Elliot and McGra...

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Detection of Vascular Dendritic Cells and Extracellular Calcium-Binding Protein S-100 in Foci of Calcification in Human Arteries.

Cited by 20 publications

References 37 publications

Expression and Cellular Localization of the CC Chemokines PARC and ELC in Human Atherosclerotic Plaques

Expression and Cellular Localization of the CC Chemokines PARC and ELC in Human Atherosclerotic Plaques

Calcification in atherosclerotic plaque of human carotid arteries: associations with mast cells and macrophages

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

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