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Furthermore order super cialis with mastercard erectile dysfunction commercial, there are a growing number of descriptive studies delineating the presence of bone formation in the aortic valve [15 order 80 mg super cialis mastercard impotence trials, 43 purchase on line super cialis erectile dysfunction treatment pdf, 44]. These studies define the biochemical and histo logical characterization of these valve lesions. We and others, have also shown that specific bone cell phenotypes are present in calcifying valve specimens in human specimens [16, 50]. These data provide the evidence that the aortic valve calcification follows the spectrum of bone formation in calcifying tissues. The role of Lrp5/beta-catenin activation in cardiovascular calcification and osteoblast bone formation: Connection with the bone axis Bone and cartilage are major tissues in the vertebrate skeletal system, which is primarily composed of three cell types: osteoblasts, chrondrocytes, and osteoclasts. In the developing embryo, osteoblast and chrondrocytes, both differentiate from common mesenchymal pro genitors in situ, where as osteoclasts are of hematopoietic origin and brought in later by in vading blood vessels. Osteoblast differentiation and maturation lead to bone formation controlled by two distinct mechanisms: intramembranous and endochondral ossification, both starting from mesenchymal condensations. The transcription factor Cbfa1 [51] has all the attributes of a master gene differ entiation factor for the osteoblast lineage and bone matrix gene expression. During embryonic development, Cbfa1 expression precedes osteoblast differentiation and is restrict ed to mesenchymal cells destined to become osteoblast. In addition to its critical role in os teoblast commitment and differentiation, Cbfa1 appears to control osteoblast activity, i. We have shown previously that cholesterol upregulates Cbfa1 gene expression in the aortic valve and atorvastatin decreases the gene expression [6] in an animal model. We have also demonstrated that Sox9 and Cbfa1 are expressed in human degenerative valves removed at the time of surgical valve replace ment [16]. The regulatory mechanism of osteoblast differentiation from osteoblast progeni tor cells into terminally differentiated cells is via a well orchestrated and well studied pathway which involves initial cellular proliferation events and then synthesis of bone ma trix proteins, which requires the actions of specific paracrine/hormonal factors and the acti vation of the canonical Wntpathway [52]. This data supports a potential regulatory mechanism that these matrix proteins play a critical role in the development of biomineralization. To date, many of these markers have been shown to be critical in the extracellular mineralization and bone formation that develops in 268 Oxidative Stress and Chronic Degenerative Diseases - A Role for Antioxidants normal osteoblast differentiation (Fig. Rajamannan have extensive experience in osteoblast cell biology and will contribute to the translational studies in the aortic valve involving the differentiation and mineralization [53, 54]. These groups have shown in in vitro and in vivo studies that lipids decrease bone formation and increase vascular calcification. This studied correlated the-/- important understanding of chronic kidney disease with decreased bone formation rates and increase in vascular calcification. This study demonstrates that accelerated vascular cal cification found in patients with end stage renal disease may be related to multifactorial mechanisms including traditional atherosclerotic risk factors and elevated serum phosphate levels. Giachelli has also studied extensively the hypothesis of a sodium phosphate abnor mality in the vascular smooth muscle cell [61]. Her group has also shown that osteopontin expression by vascular smooth muscle cells may have an inhibitory effect in the develop ment of calcification [62] which further defines the complexity of the matrix synthesis phase of bone formation.

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