Osteoblasts alkaline phosphatase

Chitosan is a well-defined matrix and as a porous scaffold, hepatocytes were found to maintain a rounded morphology when cultured within chitosan scaffolds [27]. Results showed an increase in albumin secretion as well as urea synthesis, vital metaboHc activities of hver cells [27]. Additionally, cross-hnking chitosan gels with glutaraldehyde showed increased urea formation by hepatocytes [28]. Furthermore, chitosan has shown promise as an orthopaedic scaffold. When a sponge form of chitosan was seeded with rat osteoblasts, alkaline phosphatase production was detected, as well as bone spicules, indicating initial bone formation [29]. Also, chitosan scaffolds were found to support chondrocyte attachment and expression of extracellular matrix proteins [30]. 

Kim, L., Rao, A.V., and Rao, L.G. 2003. Lycopene II-effect on osteoblasts The carotenoid lycopene stimulates cell proliferation and alkaline phosphatase activity of SaOS-2 cells. J Med Food 6 79-86. 

Once stem cells are committed to the osteoblast lineage, proliferating osteoprogenitors become preosteoblasts, cell growth declines, and there is a progressive expression of differentiation markers by osteoblasts (Stein et al. 1996). Osteoblastic differentiation is characterized by the sequential expression of alkaline phosphatase (ALP), an early marker of osteoblastic phenotype, followed by the synthesis and deposition of collagen type I, bone matrix proteins, and glycosaminoglycans and an increased expression of os-... 

The most important organic components of bone are collagens (mainly type 1 see p.344) and proteoglycans (see p. 346). These form the extracellular matrix into which the apatite crystals are deposited (biomineralization). Various proteins are involved in this not yet fully understood process of bone formation, including collagens and phosphatases. Alkaline phosphatase is found in osteoblasts and add phosphatase in osteoclasts. Both of these enzymes serve as marker enzymes for bone cells. 

Osteomalacia is the condition in which bone becomes demineralised due to deficiency of vitamin D. In this condition parathyroid hormone (PTH) acts on the bone to maintain serum calcium, resulting in demineralisation. Serum calcium is usually normal or slightly low alkaline phosphatase levels are high, reflecting excessive osteoblast activity, and serum phosphate falls as an effect of PTH on the kidney. The same condition in children results in defects in long bone formation, and is termed rickets. 

Elias et al. [21] CNT-containing orthopedic materials Osteoblasts - inoculation on material Increase of osteoblast proliferation, increase of alkaline phosphatase activity, absence of cytotoxicity... 

The alkaline phosphatases are found in bacteria, fungi, and higher animals but not in higher plants. In E. coli alkaline phosphatase is concentrated in the peri-plasmic space. In animals it is found in the brush border of kidney cells, in cells of the intestinal mucosa, and in the osteocytes and osteoblasts of bone. It is almost absent from red blood cells, muscle, and other tissues which are not involved extensively in transport of nutrients. 

Bone contains two distinct enzymes, acid and alkaline phosphatases, which are associated with osteoclasts and osteoblasts, respectively (118). Further study of acid phosphatase and bone should be rewarding. Many... 

The only essential components of the mineral deposition mechanism that are fairly certain at this time relate to phosphate. Even for phosphate, alternative mechanisms are proposed, which are not mutually exclusive but probably function in parallel, in the regulation of different aspects of skeletal calcium transport, and to some extent provide redundancy that allows many mineral transport disorders to be survivable. Alkaline phosphatase activity is essential to produce phosphate. Its major substrate is pyrophosphate. In the absence of the alkaline phosphatase, normally highly expressed as an ectoenzyme by osteoblasts, there is little matrix mineralization... 

Schlesinger, B. E., Luder, J., and Bodian, M., Rickets with alkaline phosphatase deficiency an osteoblastic dysplasia. Arch. Disease Childhood 30, 265-276 (1955). 

Pavlin D, Dove SB, Zadro R, Gluhak-Heinrich J. Mechanical loading stimulates differentiation of periodontal osteoblasts in a mouse osteoinduction model Effect on type I collagen and alkaline phosphatase genes. Calcif Tissue Int. 2000 67(2) 163-172. 

Nitric oxide (NO) is considered to be a factor that participates significantly in bone remodeling, especially as a mediator of cytokines, and their activities in bone tissue. In cell cultures, the presence of NO leads to an increase of activity of alkaline phosphatase, and to an increase of the number of calcified nodules in the primary line of bone osteoblasts (C3). Low NO concentration, on the other hand, led to increased osteoclast formation. Damoulis and Hauschka (Dl) arrived at a similar conclusion the proinflammatory cytokines induce production of NO in various types of cells, including osteoblasts and osteoclasts. It is obvious that each of these cytokines can interfere in the process of bone remodeling independently of the permissive effect of NO. 

Activity of the cells participating in bone remodeling. Usually it is the activity of the specific enzymes characteristic for the osteoblasts (especially alkaline phosphatase and its bone isoenzyme) or the osteoclasts, respectively (acid phosphatase or its bone isoenzyme)... 

Alkaline phosphatase is an enzyme of the cellular membranes. Its isoforms can be found in liver, digestive tract, placenta, and some tumor tissues. Bone isoform, BALP, is a membrane enzyme of the osteoblasts. Bone, liver, and intestinal isoforms are the posttranslational modifications of the same isoenzyme exprimed by the same gene, and the difference among them lies in various ways of reaction with a saccharide component, sialic acid (M9). 

Yl. Yamada, T., Kamiya, N., Harada, D., andTakagi, M., Effect of transforming growth factor-beta 1 on the gene expression of decorin, biglycan, and alkaline phosphatase in osteoblast precursor cells and more differentiated osteoblast cells. Histochem. J. 31, 687-694 (1999). 

It comes as no great surprise that trace elements may affect the growth and development of bone. Trace element deficiences profoundly alter hone metabolism in animals either directly or indirectly (3). The absence of a trace element in the diet can lead to inefficient functioning of a specific enzyme or enzymes that require the transition element as a cofactor. An example of this is the role of Cu and iron (Fe) in the cross-linking of collagen and elastins (4-9). The participation of Mn in the biosynthesis of mucopolysaccharides (10-12) is another example. Zn deficiency causes a reduction in osteoblastic activity, collagen and chondroitin sulfate synthesis and alkaline phosphatase activity (13-16). 

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