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At least 217 records · Page 12Linked to original sources
PubMed2002

Novel insights into uremic vascular calcification: role of matrix Gla protein and alpha-2-Heremans Schmid glycoprotein/fetuin.

Cardiovascular mortality is markedly increased in the dialysis population when compared to non-uremic subjects. Vascular and valvular calcifications are most frequently found in dialysis patients at risk and are independent predictors of cardiovascular death in this population. Traditionally, the presence of hyperphosphatemia and an increased calcium x phosphate product was considered a major pathomechanistic condition leading to excessive vascular and soft-tissue calcifications in uremic subjects. Recent studies in knockout mice, however, revealed that deficiencies in calcium-regulatory proteins may also directly contribute to the development of extraosseus calcifications. alpha(2)-Heremans Schmid glycoprotein and matrix Gla protein are important inhibitors of calcification in vivo and there is novel evidence available that a deficiency in such proteins is involved in the pathogenesis of cardiovascular calcifications in dialysis patients.

Animals↗
PubMed2000

Tumor necrosis factor-alpha promotes in vitro calcification of vascular cells via the cAMP pathway.

BACKGROUND: Vascular calcification is an ectopic calcification that commonly occurs in atherosclerosis. Because tumor necrosis factor-alpha (TNF-alpha), a pleiotropic cytokine found in atherosclerotic lesions, is also a regulator of bone formation, we investigated the role of TNF-alpha in in vitro vascular calcification. METHODS AND RESULTS: A cloned subpopulation of bovine aortic smooth muscle cells previously shown capable of osteoblastic differentiation was treated with TNF-alpha, and osteoblastic differentiation and mineralization were assessed. Treatment of vascular cells with TNF-alpha for 3 days induced an osteoblast-like morphology. It also enhanced both activity and mRNA expression of alkaline phosphatase, an early marker of osteoblastic differentiation. Continuous treatment with TNF-alpha for 10 days enhanced matrix mineralization as measured by radiolabeled calcium incorporation in the matrix. Pretreatment of cells with a protein kinase A-specific inhibitor, KT5720, attenuated cell morphology, the alkaline phosphatase activity, and mineralization induced by TNF-alpha. Consistent with this, the intracellular cAMP level was elevated after TNF-alpha treatment. Electrophoretic mobility shift assay demonstrated that TNF-alpha enhanced DNA binding of osteoblast specific factor (Osf2), AP1, and CREB, transcription factors that are important for osteoblastic differentiation. CONCLUSIONS: These results suggest that TNF-alpha enhances in vitro vascular calcification by promoting osteoblastic differentiation of vascular cells through the cAMP pathway.

Alkaline Phosphatase↗
PubMed2000

Role of vitamin K and Gla proteins in the pathophysiology of osteoporosis and vascular calcification.

Among the proteins known or suspected to be involved in bone and vascular biology are several members of the vitamin K-dependent or Gla protein family. This review focuses on the role of two of these: osteocalcin and matrix Gla protein. Osteocalcin metabolism has been implicated in the pathogenesis of osteoporosis through an unknown mechanism that may be linked to suboptimal vitamin K status resulting in its undercarboxylation and presumed dysfunction. Recent studies that have investigated this hypothesis are discussed, as are recent promising clinical studies of vitamin K supplementation in osteoporosis. A recently delineated function of matrix Gla protein is as a powerful inhibitor of calcification of arteries and cartilage. In the period covered by this review there have been several landmark studies using cell systems, whole animals and genetic techniques that have consolidated and extended our knowledge of the role of matrix Gla protein in the prevention of ectopic calcification.

Bone and Bones↗
PubMed2005

Arteriosclerosis, vascular calcifications and cardiovascular disease in uremia.

PURPOSE OF REVIEW: Arterial calcification in chronic kidney disease (CKD) is associated with increased cardiovascular risk. The mechanisms responsible for arterial calcification include alterations of mineral metabolism and expression of mineral-regulating proteins. RECENT FINDINGS: Arterial calcification is similar to bone formation, involving differentiation of vascular smooth muscle cells (VSMCs) into phenotypically distinct osteoblast-like cells. Elevated phosphate and/or calcium trigger a concentration-dependent increase of calcium precipitates in VSMC in vitro. The calcification is initiated by VSMC release of membrane-bound matrix vesicles and formation of apoptotic bodies. The presence of serum prevents these changes, indicating the presence of calcification inhibitors. Arterial calcification occurs in two sites: the tunica intima and tunica media. Intimal calcification is a marker of atherosclerotic disease and is associated with arterial stenotic lesions. Medial calcification influences outcome by promoting arterial stiffening whose principal consequences are left-ventricular hypertrophy and altered coronary perfusion. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in CKD patients. Age, duration of dialysis, smoking and diabetes are risk factors for the development of arterial calcification in end-stage renal disease. Oversuppression of parathyroid hormone and low bone turnover potentiate the development of arterial calcification. SUMMARY: Arterial disease in CKD patients is characterized by extensive calcification. Evidence has accumulated pointing to the active and regulated nature of the calcification process. Elevated phosphate and calcium may stimulate sodium-dependent phosphate cotransport involving osteoblast-like changes in cellular gene expression. Arterial calcification is responsible for stiffening of the arteries with increased left-ventricular afterload and abnormal coronary perfusion as the principal clinical consequences.

Animals↗
PubMed2003

[Diabetic angiopathy and the progression of vascular calcification].

The frequency of atherosclerotic diseases in diabetes is very high. In the occurrence of atherosclerosis the severity of diabetes is not so important. The mild diabetic condition with obesity will be a strong factor to relate with atherogenesis. As mentioned above the atherogenesis in diabetes is slightly complicated, because multiple risk factors accumulate in diabetes mellitus. These factors are hyperglycemia, hyperlipidemia, hypertension, smoking, and obesity, It has been clarified that the mechanism of arterial calcification will be same as in bone calcification process which is regulated by the various bone metabolic factors. In diabetes mellitus the characteristic vascular changes is that there is multiple calcification in the various arteries including aorta, coronary artery, and peripheral arterioles. It is considered that the necrosis and apoptosis of vascular smooth muscle cells and the transforming of vascular cells to bone cell or cartilage cell are induced and related to arterial calcification. The other factor of calcification would be inflammatory changes related to atheroma formation.

English Abstract↗
PubMed2002

The involvement of matrix glycoproteins in vascular calcification and fibrosis: an immunohistochemical study.

Calcification and fibrointimal proliferation are associated with advanced complicated atherosclerosis in large arteries but may also occur in smaller vessels, resulting in ischaemic tissue necrosis. This study investigates whether the mechanisms of calcification and intimal fibrosis are similar in vessels of different sizes. The localization of osteopontin (OPN), matrix Gla protein (MGP), thrombospondin-1 (TSP-1), and cartilage oligomeric matrix protein (COMP) was investigated in three types of human vascular lesions: atherosclerosis, chronic vascular rejection (CVR) in renal allografts, and calcific uraemic arteriolopathy (calciphylaxis). These lesions were chosen as they affect different sized blood vessels and they exhibit a fibroproliferative intimal reaction, with or without calcification, resulting in luminal obliteration and ischaemic complications. OPN, MGP, TSP-1, and COMP were not detected in normal blood vessels. However, OPN and MGP were expressed at sites of calcification within atherosclerotic lesions and in microvessels in calciphylaxis, suggesting that calcification in different sized vessels may occur by a common mechanism. These proteins were not detected in areas of fibrointimal proliferation. In contrast, TSP-1 was localized primarily within the fibrous tissue of atherosclerotic lesions and was also expressed in the expanded fibrous intima of arteries showing CVR. COMP was localized primarily within the fibrous tissue under the lipid core of the majority of advanced atherosclerotic lesions. TSP-1 and COMP were also detected in areas of microcalcification in atherosclerotic lesions and TSP-1 was detected adjacent to areas of calcification in calciphylaxis. However, neither TSP-1 nor COMP was localized to calcific foci within these lesions. The localization of OPN, MGP, TSP-1, and COMP to pathological, but not normal arterial intima supports a pathogenetic role for these proteins in the development of vascular fibrosis and calcification. Modulation of their production and activity may offer a novel approach to the therapy of a number of vascular diseases.

Adult↗
PubMed1980

[Cardiac findings and vascular calcification in arteriosclerotic obstructive disease in the pelvis and leg region. I].

In 117 patients with angiographically ascertained arteriosclerotic obstructive disease in the region of pelvis and leg the smoking of cigarettes in a high degree confirmed itself as atherogenic factor of risk. The rate of hypertension of patients with vascular disease was increased in comparison with the average population. In contrast to a control group of test persons who after clinical angiological examination did not give a clue to a vascular disease the patients with vascular diseases shows a significantly higher percentage of radiologically visible calcifications in the region of the abdominal aorta, the iliacal and the peripheral arteries of the legs. The calcification of the vessels were generalized in 85%. Apart from the calcification of the abdominal aorta the sclerosis was visible above all in the vascular are switched after the obstruction. There were no differences between normotonic and hypertonic patients with vascular diseases concerning the state of sclerosis. Clear correlations between the proof of sclerosations of the vessels and the apparative angiologically measurable narrowing of the vascular system are not known. Nevertheless in our opinion the calcification of the arteries of the legs in younger patients may be regarded as a reference to a disturbance of the arterial blood supply which must be clarified. The densitometrically established content of calcium salt in the calcaneus showed a dependance on the formation of collaterals and the state of sclerosis in the corresponding type of obstruction and may give a quantitative measure for the degree of severity of an ischaemic osteoporosis.

Age Factors↗
PubMed1977

[Gastro-intestinal bleeding and vascular calcification in pseudoxanthoma elasticum (author's transl)].

Pseudoxanthoma elasticum is an hereditary disease of elastic fibres affecting the skin, eyes and the cardio-vascular system. The radiologist should be familiar with this disease; the vascular changes can lead to bleeding from the gastrointestinal tract, which can be elucidated angiographically. There may also be circulatory disturbances in the extremities associated with early and pronounced calcification of the media and intima.

Angiography↗
PubMed2002

Cellular component of vascular calcification. Fibroblasts are essential for calcium deposition in cultured cells.

It has been reported that calcium deposition and calcium content in cultured human aortic smooth muscle cells (SMC) increased when the cells are incubated in a medium with a high phosphate concentration (2 mM). To determine the cellular components or soluble factors contributing to the deposition, we cultured commercially available SMC, fibroblasts (Fb) and endothelial cells (Ed). These cells and their mixtures were incubated for 10 days in normal or high-phosphate media. Calcium crystals were stained by the von-Kossa staining and counted in the defined area. Calcium content was measured by a colorimetric assay. SMC were incubated in high-phosphate media (up to 2 mM) or beta-glycerophosphate (beta-GP) media, resulting in no obvious deposition of calcium crystals, irrespective of the coating of type I collagen on the dish. Next, various combinations of cells were cultured, and a significant number of depositions were observed only when Fb were included in the combination. The calcium content was significantly higher in cultures of SMC and Fb. The calcium deposition on single or mixture of the cells did not increase compared with control when cells were incubated in a high concentration of phosphate, cultured in the existence of beta-GP or uremic serum. We therefore conclude that Fb, rather than SMC or Ed, are essential for calcium deposition and calcium accumulation in culture. Phosphate concentration in the medium and uremic serum did not influence the deposition of calcium.

Calcification, Physiologic↗