Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibroblastic colonies, each of which is derived from a single precursor cell (CFU-F), are formed when suspensions of marrow cells are cultured in vitro. The ability of marrow CFU-F to differentiate in vitro was investigated using the expression of alkaline phosphatase activity as a marker for osteogenic differentiation. In cultures of rabbit marrow cells the colonies formed varied in size, morphology and expression of enzyme activity, indicating that marrow stromal CFU-F are a heterogeneous population. Growth and differentiation of marrow CFU-F can be modified in vitro. Epidermal growth factor increased average colony size and reduced clonal expression of alkaline phosphatase activity to very low levels. Hydrocortisone activated the osteogenic differentiation programme within the cellular progeny of a wide spectrum of CFU-F. The results support the possible development of in vitro clonal methods for the study of differentiation and regulation of the osteogenic and other fibroblastic cell lines of the marrow stromal system.
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PMID:Clonal analysis in vitro of osteogenic differentiation of marrow CFU-F. 349 42

The increase in alkaline phosphatase in asynchronous cultures of HeLa S(3) cells grown in medium supplemented with hydrocortisone is characterized by a lag period of 10-12 hr. Present studies utilizing synchronous cell populations indicate: (a) a minimum of 8-10 hr of incubation with hydrocortisone is necessary for maximum induction of alkaline phosphatase; (b) the increase in enzyme activity produced by hydrocortisone is initiated exclusively in the synthetic phase of the cell cycle; (c) alkaline phosphatase activity does not vary appreciably over a normal control cell cycle. Radioactive hydrocortisone is rapidly distributed into HeLa cells irrespective of their position in the cell cycle, indicating that inductive effects are not governed by selective permeability during the cell cycle. Hydrocortisone-1,2-[(3)H] diffuses back from the cell into the medium when the cells are incubated in fresh medium containing no hydrocortisone, and the alkaline phosphatase induction, under these conditions, is completely reversible.
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PMID:Cell cycle events in the hydrocortisone regulation of alkaline phosphatase in HeLa S3 cells. 576 19

Na+,K+-ATPase, HCO3(-)-ATPase, Ca2+,Mg2+,-ATPase, Ca2+-ATPase, and alkaline phosphatase activities were measured in cultures of osteoblastlike cells treated with fluoride and cortisol separately and in combinations. Low concentrations of cortisol increased HCO3- -ATPase (10(-11) to 10(-18) M cortisol) and alkaline phosphatase (10(-11) to 10(-9) M cortisol) activities, but higher cortisol concentrations reduced these activities. Na+,K+-ATPase, Ca2+,Mg2+-ATPase, and Ca2+-ATPase activities tended only to be reduced by cortisol. Fluoride (10(-6) and 5 X 10(-6) M) increased HCO3(-)-ATPase and alkaline phosphatase activities, but these activities were similar to controls in the presence of 10(-5) M fluoride. Ca2+,Mg2+-ATPase activity was decreased and Na+,K+-ATPase activity was increased as the concentration of fluoride increased (10(-6) to 10(-5) M). Preliminary experiments with fluoride indicated that lower concentrations (10(-7) M) were without effect. Cortisol concentrations of 10(-9) and 10(-8) M were chosen for studies with combinations of cortisol and fluoride because the effects of these concentrations on alkaline phosphatase activity were opposite, i.e. 10(-9) M increased whereas 10(-8) M decreased activity. Fluoride concentrations of 10(-6), 5 X 10(-6), and 10(-5) M were chosen because a peak of alkaline phosphatase activity occurred at 5 X 10(-6) M fluoride. Higher (10(-4) M) and lower (10(-7) M) fluoride concentrations were without effect. The effects of combinations of cortisol and fluoride depend on the enzyme activity measured. Fluoride (10(-6) M) combined with cortisol (10(-9) M) produced a peak of Na+,K+-ATPase activity. The increased activity obtained with all concentrations of fluoride alone was preserved when fluoride was combined with 10(-8) M cortisol, although the activity tended to be reduced at 5 X 10(-6) and 10(-5) M fluoride. HCO3(-)-ATPase activity was increased by fluoride combined with 10(-8) M cortisol and decreased by fluoride combined with 10(-9) M cortisol compared to the activities obtained with fluoride alone. The decrease in Ca2+,Mg2+-ATPase activity caused by fluoride alone was prevented by 10(-9) and enhanced by 10(-8) M cortisol, although all treatments produced the same activity at 10(-5) M fluoride. Ca2+-ATPase activity tended to be increased by combinations of fluoride and cortisol, but significantly so only at 10(-5) M fluoride in combinations with 10(-8) and 10(-9) M cortisol.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of cortisol and fluoride on ion-transporting ATPase activities in cultured osteoblastlike cells. 609 29

The influence of hydrocortisone (10(-8)--10(-5) M) and thyroxine (10 (-9)--10(-6) M) on intestinal epithelial cell differentiation and proliferation have been studied using explants of suckling mouse jejunum maintained in serum-free organ culture. Hydrocortisone induced the appearance of sucrase activity and increased trehalase, glucoamylase, lactase and alkaline phosphatase activities. Thyroxine was completely ineffective at all the concentrations used. None of these hormones affected the mitotic activity or the 3H-thymidine incorporation into DNA. These results demonstrate that hydrocortisone but not thyroxine acts directly on intestinal brush border membrane differentiation and that both hormones do not influence the proliferation of the epithelial cells during postnatal development.
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PMID:Comparative study of the effect of hydrocortisone and thyroxine on suckling mouse small intestine in organ culture. 614 44

The s.c. administration of cortisol to hamsters (50 mg/kg body wt/day for 4 days) produces a significant increase in maltase sucrase, alkaline phosphatase and leucineaminopeptidase activity in intestinal mucosa. Lactase activity is unaffected by cortisol. Gamma-glutamyltranspeptidase activity increases slightly in females but remains unchanged in males. Cortisol causes increase in proline and glycine absorption without changing the absorption of lysine.
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PMID:The effect of cortisol on stimulation of enzymatic activity and absorption of amino acids in the small intestine of adult hamsters. 615 Jul 87

Incubation of HeLa cells with 10-80 mM ethanol, caused a dose-dependent decrease in alkaline phosphatase specific activity. With 80 mM ethanol, the decrease became apparent after 24-48 hr incubation. The same dose-dependent effect was observed with the nonmetabolizable alcohol t-butanol. The effect of ethanol was not due to toxicity as the cells continued to replicate for weeks in the presence of ethanol and was reversible. There were no differences in the Km values of alkaline phosphatase in crude extracts or solubilized enzyme prepared either from control or 80 mM ethanol-treated cells. Hydrocortisone and choline chloride, which by themselves increase alkaline phosphatase specific activity, altered the effect of ethanol on alkaline phosphatase. In the presence of either 1 microM hydrocortisone or 40 mM choline chloride, neither 10 nor 20 mM ethanol decreased alkaline phosphatase specific activity.
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PMID:Effect of ethanol on alkaline phosphatase activity in HeLa cells. 634 20

The effect of hydrocortisone (75 mg/kg) on antral, duodenal and pancreatic gastrin concentrations and on intestinal lactase, sucrase, maltase and alkaline phosphatase activities was investigated in suckling rats. Antral and pancreatic gastrin levels in normal 4- to 22-day-old rats were also determined. Hydrocortisone was injected daily to 7- and 10-day-old rats for 6 days. At the end of the experimental period the animals were 12 and 15 days old. Control groups were injected with saline. Hydrocortisone administration caused a profound induction in sucrase activity and markedly stimulated maltase and alkaline phosphatase activities in both age groups. After hydrocortisone administration 12-day-old rats showed a slight (28%) but significant stimulation in lactase activity, whereas in 15-day-old rats the enzyme activity was significantly decreased by 23%, compared to the respective saline control. Gastrin concentration in the antrum increased steadily between 4 and 22 days of age, whereas in the pancreas it decreased sharply from a relatively high level in 4-day-old rats to an essentially undetectable level in 22-day-old rats. Following hydrocortisone administration gastrin concentration in the antrum of 12- and 15-day-old rats was found to be significantly increased by 104 and 47%, respectively, but in the pancreas it decreased by 44 and 57%, when compared with the corresponding saline control. Hydrocortisone caused no apparent change in duodenal gastrin concentration in 12-day-old rats but produced a nonsignificant 35% increment in 15-day-old animals. The observed changes after hydrocortisone treatment are thought to be the result of an early maturation of the gastrointestinal mucosa and pancreas by the steroid.
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PMID:Effect of hydrocortisone on gastrin cell function in various tissues of suckling rats. 641 68

The effects of cortisol on bone formation are complex and may be modulated by the presence of periosteal cells or by factors released by the periosteal tissue. To test these possibilities, cortisol was examined for its effects on the incorporation of 3H-proline into collagenase-digestible protein (CDP) and noncollagen protein (NCP), on DNA synthesis and on alkaline phosphatase activity in intact and in the periosteum and nonperiosteal bone of dissected calvariae from 21-day-old fetal rats. After 24 h of treatment, cortisol increased the incorporation of 3H-proline into CDP in intact bones and in the nonperiosteal bone of calvariae dissected after the culture. Cortisol inhibited the incorporation of 3H-thymidine into calvarial DNA but it caused a small increase in nonperiosteal DNA content. Cortisol did not affect the incorporation of 3H-proline into CDP in calvariae dissected prior to the culture if the periosteum and nonperiosteal central bone were incubated separately; the stimulatory effect was observed only if the two tissues were cultured in the same vial and were in contact. In contrast, cortisol stimulated alkaline phosphatase activity in the central nonperiosteal bone of calvariae dissected before or after the culture. After 72-96 h of treatment, cortisol inhibited the labeling of CDP, NCP, and DNA and the DNA content in intact bones and in both periosteal and nonperiosteal central bone of calvariae dissected after the culture. In contrast, when the periosteum was removed before the incubation, these inhibitory effects were observed in the periosteum and not in the nonperiosteal bone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cortisol on periosteal and nonperiosteal collagen and DNA synthesis in cultured rat calvariae. 643 Apr 99

Glucocorticoid-induced osteoporosis is believed to be caused by increased bone resorption and decreased bone formation. However, the direct effects of glucocorticoids on bone formation are, as yet, not fully understood. Cortisol, corticosterone, and dexamethasone were examined for their effects on alkaline phosphatase activity, the incorporation of [3H]proline into type I collagen, DNA content, and mitotic index in intact 21-day-old fetal rat calvariae. After 24 h of treatment, cortisol at 1-100 nM increased the incorporation of [3H]proline into type I collagen, whereas at 1-10 microM, cortisol inhibited type I collagen labeling. After 96 h, cortisol (0.1-10 microM) had an inhibitory effect on type I collagen labeling and alkaline phosphatase activity. Cortisol had a small, not dose dependent, and transient stimulatory effect on alkaline phosphatase which appeared after 12-24 h of exposure, whereas the inhibitory effect was dose related, it appeared and was near-maximal after 48 h of continuous treatment with cortisol. Corticosterone and dexamethasone had an effect similar to that of cortisol on type I collagen synthesis and alkaline phosphatase activity. None of the steroids tested affected the release of the enzyme into the culture medium. Cortisol, corticosterone, and dexamethasone did not alter calvarial DNA content after 24 h of treatment, but after 96, concentrations of 1 nM to 10 microM were inhibitory. The decrease in DNA appeared after 48 h of exposure to 100 nM cortisol and was maximal after 72 h. Histological sections showed a marked and generalized decrease in the number of mitoses after colcemid arrest in calvariae treated with 100 nM cortisol, corticosterone, or dexamethasone for 96 h. These studies indicate that glucocorticoids have a dual effect on type I collagen synthesis and alkaline phosphatase activity in cultured calvariae: a transient stimulatory effect after short term treatment and an inhibitory one after long term exposure. The latter is related to a generalized decrease in cell population.
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PMID:Effect of glucocorticoids on type I collagen synthesis, alkaline phosphatase activity, and deoxyribonucleic acid content in cultured rat calvariae. 682 19

Tissue culture techniques were used to study a number of factors and mechanisms which are important in the development and metabolism of bone tissue. As an example of an external factor influencing bone development, the importance of the composition of the gasphase which is in equilibrium with the fluid bathing osteoblasts and hypertrophic chondrocytes, was investigated in cultured metatarsal bone rudiments. In vivo, one expects the presence of an O2 gradient in the cartilaginous epiphyses of long bones: low O2 tension between the nonhypertrophic chondrocytes, high O2 tension in periosteum and hypertrophic zone, bordering the marrow cavity. The in vitro findings correlated with these expectations. High CO2 (5%) and high O2 (40%) tensions stimulated calcification; in air, calcification was severely inhibited. On the other hand, maturing chondrocytes were damaged by high O2 tensions. An important cellular mechanism in calcification is the intracellular accumulation of calcium (and phosphate) in osteoblasts and hypertrophic chondrocytes which can be demonstrated with the GBHA stain of Kashiwa [9]. The extracellular role of alkaline phosphatase (AP) present on the cell membranes of these cells was shown to be a less decisive factor in calcification. In the presence of AP inhibitor in a concentration high enough to inhibit AP activity to a large extent, calcification was shown to proceed normally. The effects of a number of hormones known to be important for the development and metabolism of bone tissue was studied using tissue culture (calvaria) as well as culture of different isolated bone cells. The parathyroid hormone (PTH) induced rise of the intracellular cAMP level was found to originate primarily from the osteoblasts not the osteoclasts. Isolated osteoblasts showed a high cAMP response after PTH addition. Cortisol was shown to inhibit PTH induced resorption but to potentiate PTH induced cAMP response in calvaria. Various PTH fragments (desamino 1-34, 2-34, 3-34) were shown to be active as stimulators of bone resorption (although they were less active in this respect than the intact molecule 1-84), but did not stimulate cAMP production in calvaria or isolated osteoblasts. The results obtained strengthened the hypothesis that cAMP is not the (only) mediator in PTH induced bone resorption.
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PMID:Regulatory mechanisms in the development of bone and cartilage: the use of tissue culture techniques in the study of the development of embryonic bone and cartilage: a perspective. 715 53


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