Macrophage-Derived Matrix Vesicles

New, Sophie E. P.; Goettsch, Claudia; Aikawa, Masanori; Marchini, Júlio Flávio Meirelles; Shibasaki, Manabu; Yabusaki, Katsumi; Libby, Peter; Shanahan, Catherine M.; Croce, Kevin; Aïkawa, Elena

doi:10.1161/circresaha.113.301036

Cited by 377 publications

(235 citation statements)

References 15 publications

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“…14 21 22 In bone, matrix vesicles secreted by osteoblasts serve as initiation sites for mineral crystal formation. In human vascular and valvular calcification, matrix vesicles appear to have the same role, 23 and these may be produced by both macrophages 24 and vascular smooth muscle cells. 25 Both vascular-derived and osteoblast-derived matrix vesicles contain calcium-binding and mineralisation-regulating proteins.…”

Section: Comparison To Bone Mineralisationmentioning

confidence: 99%

Cell-matrix mechanics and pattern formation in inflammatory cardiovascular calcification

Hsu

Lim

Tintut

et al. 2016

Heart

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Calcific diseases of the cardiovascular system, such as atherosclerotic calcification and calcific aortic valve disease, are widespread and clinically significant, causing substantial morbidity and mortality. Vascular cells, like bone cells, interact with their matrix substrate not only through molecular signals, but also through biomechanical signals, such as traction forces transmitted from cytoskeleton to matrix. The interaction of contractile vascular cells with their matrix may be one of the most important factors controlling pathological mineralization of the artery wall and cardiac valves. In many respects, the matricrine and matrix mechanical changes in calcific vasculopathy and valvulopathy resemble those occurring in embryonic bone development and normal bone mineralization. The matrix proteins provide not only a microenvironment for propagation of crystal growth but also provide mechanical cues to the cells that direct differentiation. Small contractions of the cytoskeleton may tug on integrin links to sites on matrix proteins, and thereby sense the stiffness, possibly through deformation of binding proteins causing release of differentiation factors such as products of the members of the transforming growth factor-beta superfamily. Inflammation and matrix characteristics are intertwined: inflammation alters the matrix such as through matrix metalloproteinases, while matrix mechanical properties affect cellular sensitivity to inflammatory cytokines. The adhesive properties of matrix also regulate self-organization of vascular cells into patterns through reaction-diffusion phenomena and left-right chirality. In this review, we summarize the roles of extracellular matrix proteins and biomechanics in the development of inflammatory cardiovascular calcification.

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Section: Comparison To Bone Mineralisationmentioning

confidence: 99%

Cell-matrix mechanics and pattern formation in inflammatory cardiovascular calcification

Hsu

Lim

Tintut

et al. 2016

Heart

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“…Although cardiovascular calcification in the medial layer in association with CKD appears to link to long-term elevation of serum phosphate levels, apoptosis and uremic derangements [56], inflammation also acts in this process [95]. By releasing extracellular vesicles containing a phosphatidylserine-annexinV-S100A9 complex that facilitates mineral nucleation, macrophages are involved in the early, pro-inflammatory phase of calcification in atherosclerotic plaques [96]. Inflammatory cytokines, including TNF-α, IL-1 and IL-6, are associated with increased cardiovascular calcification [97, 98], and in a cohort free of clinically apparent cardiovascular disease, high C-reactive protein levels were associated with coronary artery calcification in both men and women [99].…”

Section: Possible Mechanisms By Which Hmgb1 Promotes Cardiovascular Cmentioning

confidence: 99%

Roles of High Mobility Group Box 1 in Cardiovascular Calcification

Chen¹,

Wang²,

Chen³

et al. 2017

Cell Physiol Biochem

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Calcific disease of the cardiovascular system, including atherosclerotic calcification, medial calcification in diabetes and calcific aortic valve disease, is an important risk factor for many adverse cardiovascular events such as ischemic cardiac events and subsequent mortality. Although cardiovascular calcification has long been considered to be a passive degenerative occurrence, it is now recognized as an active and highly regulated process that involves osteochondrogenic differentiation, apoptosis and extracellular vesicle release. Nonetheless, despite numerous studies on the pathogenesis of cardiovascular calcification, the underlying mechanisms remain poorly understood. High mobility group box 1 (HMGB1), a nuclear protein bound to chromatin in almost all eukaryotic cells, acts as a damage-associated molecular pattern (DAMP) when released into the extracellular space upon cell activation, injury or death. Moreover, HMGB1 also functions as a bone-active cytokine participating in bone remodeling and ectopic calcification pathogenesis. However, studies on the roles of HMGB1 in promoting cardiovascular calcification are limited to date, and the mechanisms involved are still unclear. In this review, we summarize recent studies investigating the mechanism of cardiovascular calcification and discuss multiple roles of HMGB1 in its development.

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“…Nonetheless, the precise mechanisms of vascular calcification are still under investigation. Several basic studies indicate microcalcification, the earliest form of calcification, occurs in apoptotic vascular smooth muscle cells [6,7] and macrophages in conjunction with an increase in serum calcium-phosphorous product [8]. Increases in phosphate concentration in vascular smooth muscle cells induce a switch toward an osteoblast-like phenotype.…”

Section: Figmentioning

confidence: 99%