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Alkaline phosphatase

About: Alkaline phosphatase is a research topic. Over the lifetime, 20218 publications have been published within this topic receiving 540547 citations. The topic is also known as: Alkaline_phosphatase & IPR001952.


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Journal ArticleDOI
TL;DR: Screening for mutations in the TNSALP gene allows genetic counseling and prenatal diagnosis of the disease in families with severe forms of hypophosphatasia, and screening may also be helpful in confirming diagnosis of hypophile phosphatasia when biochemical and clinical data are not clear.
Abstract: Hypophosphatasia is an inborn error of metabolism caused by a deficiency of liver-, bone- or kidney-type alkaline phosphatase due to mutations in the tissue-nonspecific alkaline phosphatase (ALPL) gene. Most of the 65 distinct mutations described to date are missense mutations, a result which must be correlated with the great variability of clinical expression ranging from stillbirth without mineralized bone to pathologic fractures developing only late in adulthood. Correlations of genotype and phenotype have been established on the basis of clinical data exhibited by the patients, transfection studies, computer-assisted modeling, and examination of biochemical properties of ALP in cultured fibroblasts of patients. Screening for mutations in the TNSALP gene allows genetic counseling and prenatal diagnosis of the disease in families with severe forms of hypophosphatasia, and screening may also be helpful in confirming diagnosis of hypophosphatasia when biochemical and clinical data are not clear. Screening is also the necessary first step in further studies to elucidate dominant transmission of the disease and of liver-, bone- and kidney-type alkaline phosphatase activity mechanism.

143 citations

Journal ArticleDOI
TL;DR: Observations indicate that glucocorticoids regulate the commitment of progenitors derived from dental pulp cells to form odontoblast-like cells, while reducing the proportion of SMA-positive cells.
Abstract: Regenerative dental pulp strategies require the identification of precursors able to differentiate into odontoblast-like cells that secrete reparative dentin after injury. Pericytes have the ability to give rise to osteoblasts, chondrocytes, and adipocytes, a feature that has led to the suggestion that odontoblast-like cells could derive from these perivascular cells. In order to gain new insights into this hypothesis, we investigated the effects of dexamethasone (Dex), a synthetic glucocorticoid employed to induce osteogenic differentiation in vitro, in a previously reported model of human dental pulp cultures containing pericytes as identified by their expression of smooth muscle actin (SMA) and their specific ultrastructural morphology. Our data indicated that Dex (10–8 M) significantly inhibited cell proliferation and markedly reduced the proportion of SMA-positive cells. Conversely, Dex strongly stimulated alkaline phosphatase (ALP) activity and induced the expression of the transcript encoding the major odontoblastic marker, dentin sialophosphoprotein. Nevertheless, parathyroid hormone/parathyroid hormone-related peptide receptor, core-binding factor a1/osf2, osteonectin, and lipoprotein lipase mRNA levels were not modified by Dex treatment. Dex also increased the proportion of cells expressing STRO-1, a marker of multipotential mesenchymal progenitor cells. These observations indicate that glucocorticoids regulate the commitment of progenitors derived from dental pulp cells to form odontoblast-like cells, while reducing the proportion of SMA-positive cells. These results provide new perspectives in deciphering the cellular and molecular mechanisms leading to reparative dentinogenesis.

143 citations

Journal ArticleDOI
TL;DR: Results support the theory of hybrid protein formation which has been proposed to account for intra-cistron complementation and support the normal alkaline phosphatase protein is composed of two identical subunits whose structure is determined by a single functioning genetic unit.

143 citations

Journal ArticleDOI
TL;DR: Higher magnesium levels prevented BVSMC calcification, inhibited expression of osteogenic proteins, apoptosis and further progression of already established calcification and may have the potential to play a role for VC also in clinical situations.
Abstract: Background. Vascular calcification (VC), mainly due to elevated phosphate levels, is one major problem in patients suffering from chronic kidney disease. In clinical studies, an inverse relationship between serum magnesium and VC has been reported. However, there is only few information about the influence of magnesium on calcification on a cellular level available. Therefore, we investigated the effect of magnesium on calcification induced by b-glycerophosphate (BGP) in bovine vascular smooth muscle cells (BVSMCs). Methods. BVSMCs were incubated with calcification media for 14 days while simultaneously increasing the magnesium concentration. Calcium deposition, transdifferentiation of cells and apoptosis were measured applying quantification of calcium, von Kossa and Alizarin red staining, real-time reverse transcription–polymerase chain reaction and annexin V staining, respectively. Results. Calcium deposition in the cells dramatically increased with addition of BGP and could be mostly prevented by co-incubation with magnesium. Higher magnesium levels led to inhibition of BGP-induced alkaline phosphatase activity as well as to a decreased expression of genes associated with the process of transdifferentiation of BVSMCs into osteoblast-like cells. Furthermore, estimated calcium entry into the cells decreased with increasing magnesium concentrations in the media. In addition, higher magnesium concentrations prevented cell damage (apoptosis) induced by BGP as well as progression of already established calcification. Conclusions. Higher magnesium levels prevented BVSMC calcification, inhibited expression of osteogenic proteins, apoptosis and further progression of already established calcification. Thus, magnesium is influencing molecular processes associated with VC and may have the potential to play a role for VC also in clinical situations.

143 citations

Journal ArticleDOI
TL;DR: In this article, the pH stability of urease, acid phosphatase, alkaline phosphatases and phosphodiesterase was investigated by first incubating a soil sample at the indicated pH (1−13) for 24 h and then measuring the activity at its optimal pH under standardized conditions.
Abstract: The pH stability of urease, acid phosphatase, alkaline phosphatase and phosphodiesterase in soils was investigated by first incubating a soil sample at the indicated pH (1–13) for 24 h and then measuring the activity at its optimal pH under standardized conditions. Generally, the decline in enzyme activity in a pH-profile near the optimum pH range was due to a reversible reaction that involved ionization or deionization of acidic or basic groups in the active centre of the enzyme-protein. Irreversible inactivation of the enzyme was particularly evident at the lower and higher ranges of acidic and alkaline conditions. Results showed that the pH stability of soil enzymes was highly dependent on the soils being assayed. The variation among soils may be attributed to the diversity of vegetation, micro-organisms and soil fauna as sources contributing to the enzyme activity and to the protective sites which allowed entrapment of the enzyme within colloidal humus and organo-mineral complexes. Adherence of the enzyme-protein to the humic-clay fractions would allow some resistance to pH denaturation.

142 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
2023795
20221,761
2021271
2020302
2019294