Ectopic calcification: new concepts in cellular regulation

Giachelli, Cecilia M.

doi:10.1007/s003920170039

Cited by 55 publications

(38 citation statements)

References 18 publications

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“…87,100 -103 Because of its beneficial anticalcific affects and ability to promote mineral resorption, OPN is currently being considered as a potential local therapeutic to limit or remove pathological mineralization in cardiovascular settings such as native valve repair and bioprosthetic valve material development. 104,105 …”

Section: Remodeling and Biomineralizationmentioning

confidence: 99%

Osteopontin

Scatena

Liaw

Giachelli

2007

ATVB

579

245

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Abstract-Osteopontin (OPN) is a multifunctional molecule highly expressed in chronic inflammatory and autoimmune diseases, and it is specifically localized in and around inflammatory cells. OPN is a secreted adhesive molecule, and it is thought to aid in the recruitment of monocytes-macrophages and to regulate cytokine production in macrophages, dendritic cells, and T-cells. OPN has been classified as

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Section: Remodeling and Biomineralizationmentioning

confidence: 99%

Osteopontin

Scatena

Liaw

Giachelli

2007

ATVB

579

245

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“…Results from several in vitro studies have indicated that Pi stimulates SMC to undergo phenotypic changes that predispose them to calcification (21)(22)(23). The transcription factor corebinding factor-1 (Cbfa-1) has been found to regulate osteocalcin, osteopontin, and type I collagen gene expression.…”

Section: Mechanistic Evidence For Hyperphosphatemiainduced Calcificationmentioning

confidence: 99%

Vascular Calcification

Giachelli

2003

Journal of the American Society of Nephrology

275

204

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Abstract. Uremic patients are prone to widespread ectopic extraskeletal calcification resulting from an imbalance of systemic inorganic phosphate (Pi). There can be serious consequences of this process, particularly when it results in the calcification of the vasculature. A recent study examined the response of cultured human aortic smooth muscle cells to varying levels of extracellular Pi. Cells that were exposed to Pi levels similar to those seen in uremic patients (Ͼ1.4 mmol/L) showed dose-dependent increases in cell culture calcium deposition. The results of this study also defined the role of elevated phosphate in transforming the vascular phenotype of these cells to an osteogenic phenotype, such that a predisposition for calcification was created. Pi-induced changes included increased expression of the osteogenic markers osteocalcin and core-binding factor-1 genes, the latter of which is considered a "master gene" critical for osteoblast differentiation. These changes occur early after exposure to high phosphate levels and seem to be mediated by a sodium-dependent phosphate co-transporter, Pit-1 (Glvr-1

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“…14 Although elastin is a primary constituent of cardiovascular tissues, its precise role in pathological vascular calcification remains speculative, perhaps because of the multifactorial nature of the disease processes involved. 13,15,16 Purified elastin, however, calcifies very rapidly in animal models. Our PEB implants, which are at least 95% pure elastin, were heavily calcified as early as 30 days (107.1 Ϯ 11.8 g/mg) after subdermal implantation in the adult mouse model.…”

Section: Discussionmentioning

confidence: 98%

Biocompatibility of a xenogenic elastin‐based biomaterial in a murine implantation model: The role of aluminum chloride pretreatment

Hinds¹,

Courtman²,

Goodell³

et al. 2004

J Biomedical Materials Res

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We have investigated the long-term effect of aluminum chloride (AlCl(3)) treatment on the calcification and inflammatory reaction of a porcine elastin-derived biomaterial (PEB) in a novel subdermal adult mouse model. Untreated PEB disks and PEB treated with AlCl(3) were implanted subdermally in BALB/c mice for 30, 60, and 180 days. The calcification of the elastin disks was examined with histological analysis and atomic absorption analysis of calcium content. The inflammatory reaction was evaluated both with histological analysis of explants and by an enzyme-linked immunosorbent assay of the serum in each mouse to determine the production of antielastin antibodies. Robust calcification was evident in all untreated PEBs with calcium levels of 107.1 +/- 11.8, 151.4 +/- 14.4, and 227.2 +/- 23.8 microg/mg for 30, 60, and 180 days, respectively. AlCl(3) treatment only temporarily prevented the calcification of the elastin disks for 30 days. By 60 and 180 days, the AlCl(3)-treated materials had significant calcification with 88.7 +/- 17.4 and 105.3 +/- 27.0 microg/mg calcium, respectively. The inflammatory reaction was moderate for both types of implants. The AlCl(3)-treated implants displayed significantly more macrophage and lymphocyte infiltration at 180 days after implantation, and a trend to higher humoral responses at 30 and 60 days when compared with untreated PEBs. We conclude that PEBs extensively calcify in the adult mice model. AlCl(3) treatment of elastin enhances the long-term immunological response to xenogenic elastin implants and merely delays the onset of calcification.

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Ectopic calcification: new concepts in cellular regulation

Cited by 55 publications

References 18 publications

Osteopontin

Osteopontin

Vascular Calcification

Biocompatibility of a xenogenic elastin‐based biomaterial in a murine implantation model: The role of aluminum chloride pretreatment

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