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)

Endogenous alkaline phosphatase activity has been localized histochemically on the surface of enteric neurons of the guinea-pig small intestine by both light and electron microscopy. The enzyme activity was associated with some myenteric neurons that had Dogiel type I morphology, and the histochemical reaction products typically formed a honeycomb-like structure on labelled cell bodies. No Dogiel type II neurons in the myenteric plexus or submucous neurons showed alkaline phosphatase reactivity. Nerve fibres reactive for alkaline phosphatase were present in the myenteric plexus and ran in bundles in the circular muscle and deep muscular plexus. In addition, reactive varicose axons supplied the submucous plexus and non-ganglionated plexus of the mucosa. The results of interruption of the enteric neuronal pathways demonstrated that alkaline phosphatase-reactive myenteric neurons project anally to other myenteric ganglia, to the circular muscle and to the submucous plexus. Sequential enzyme histochemistry showed that virtually all alkaline phosphatase-reactive neurons also contained nitric oxide synthase, revealed by NADPH-diaphorase reactivity. It was estimated that 14-18% of all myenteric neurons showed alkaline phosphatase reactivity. About one-third of nitric oxide synthase-containing myenteric neurons, however, did not contain alkaline phosphatase activity. At the ultrastructural level, alkaline phosphatase activity was associated specifically with the plasma membranes of nerve cell bodies, axons and dendrites of some myenteric neurons. Reactive nerve fibres made close appositions with non-reactive submucous neurons and, within myenteric ganglia, predominantly with other alkaline phosphatase-reactive neurons. In addition to its presence in neurons, alkaline phosphatase reactivity was also present in some endothelial cells in blood vessels in the submucosa and in capillary pericytes. It is concluded, on the basis of the projections and neurochemistry, that in the guinea-pig small intestine alkaline phosphatase activity is associated with nitric oxide synthase-containing neurons which include inhibitory motor neurons to the circular muscle, and anally-directed interneurons to other myenteric and submucous neurons.
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PMID:Characterization of alkaline phosphatase-reactive neurons in the guinea-pig small intestine. 753 94

The NADPH-diaphorase (NADPH-d) reaction is frequently used to visualize the diaphorase activity of nitric oxide synthase (NOS). However, this tetrazolium salt procedure can be of limited specificity at sites where non-specific alkaline phosphatase (alP) and NADHd activity co-exist. This is shown in the present paper using methods of catalytic histochemistry for these three enzymes and levamisole as alP inhibitor for certain mouse tissues. In the urothelium, portio, vaginal and endometrial epithelium as well as in some smooth muscle cells alP hydrolyzes NADPH to NADH which in turn serves as substrate for NADHd leading to false-positive formazan production. To exclude this possibility, it is recommended always to include levamisole in the incubation medium if the NADPHd activity of NOS has to be investigated.
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PMID:Nonspecific alkaline phosphatase activity can be responsible for staining of NADPH-diaphorase activity in certain non-neural cells. 755 70

The effect of nitric oxide (NO) on osteoblastic differentiation was examined in cultured mouse osteoblasts. Interleukin-1beta and tumor necrosis factor-alpha expressed inducible NO synthase gene with little effect on constitutive NO synthase gene. These cytokines increased NO production, which was inhibited by L-NMMA pretreatment, and decreased alkaline phosphatase (AIPase) activity, which was not restored by L-NMMA. Furthermore, NO donors, sodium nitroprusside and NONOate dose-dependently elevated AIPase activity and expression of osteocalcin gene. These results suggest that NO directly facilitates osteoblastic differentiation and the cytokine-induced inhibition of AIPase activity is mediated via mechanism other than NO.
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PMID:Direct action of nitric oxide on osteoblastic differentiation. 923 37

The aim of this study was to assess the involvement in decidual proliferation of nitric oxide (NO), a regulator of many cellular processes, that is synthesized from L-arginine by NO synthase. The investigation was conducted on pseudopregnant (PG) rats in which the decidual cell reaction, the basis for the decidualization process, was surgically induced by uterine trauma on PG Day 4. Groups of animals (n = 5) were pretreated with either 2 doses/day of N(G)-nitro-L-arginine methyl ester (L-NAME) that inhibits NO synthase, or twice daily doses of L-NAME plus L-arginine combined. Drug application times coincided with 3 hr after lights on or 3 hr before lights off. The two treatment regimens (PG Days 1-4 or 5-8) respectively preceded or followed decidual induction. Animals were sacrificed at mid-light on PG Day 9, the day of maximal growth response to the deciduogenic stimulus. Parallel, time-dependent increases in both NO synthase activity and decidual growth occurred mainly in the endometrium. L-NAME produced reductions in endometrial and myometrial growth that were reversed by the combined L-NAME plus L-arginine treatments. These inhibitory effects by L-NAME were caused by only the pretraumal (PG Days 1-4) administration. Hormonally, circulating progesterone levels were similarly affected by this early treatment and may also contribute to the reduced decidual sensitivity. In contrast, serum estradiol, along with the zinc metalloenzymes, alkaline phosphatase and the matrix metalloproteinases--prominent decidualization biomarkers--were all unaffected by either the pre- or post-decidual induction dosings. The study demonstrates that inducible NO synthase/endogenous NO may physiologically participate in uterine metabolism during the decidual cell reaction. Moreover, by virtue of L-NAME inhibition of the decidual response, it appears that NO synthase/NO may influence decidual growth either by directly increasing uterine sensitivity to the deciduogenic stimulus or by indirectly affecting endometrial vascularity and subsequent availability of decidual metabolites.
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PMID:Antiproliferative effects of inducible nitric oxide synthase inhibition on decidualization in pseudopregnant rats. 957 51

We investigated the enzymes involved in the NADPH-diaphorase (d) reaction in the rat and pig bladder urothelium. The urothelial cell layer displayed intense and uniform NADPH-d activity. Preincubation with the flavoprotein inhibitor diphenyleneiodionium chloride (DPI) and the alkaline phosphatase inhibitor levamisole concentration-dependently decreased the urothelial NADPH-d activity. Immunoreactivities to neuronal (n), endothelial (e), or inducible (i) nitric oxide synthase (NOS) were not detected in rat or pig urothelial cells. In rats, the urothelium was uniformly immunoreactive for NADPH cytochrome P450 reductase, whereas the pig urothelium displayed inconsistent labeling. In lipopolysaccharide (LPS)-treated rats, the bladder urothelium showed positive iNOS immunoreactivity. The iNOS labeling was found predominantly in cells located in the basal layer of the urothelium. In the pig bladder mucosa, a Ca2+-dependent NOS activity was evident in cytosolic and particulate fractions that was quantitatively comparable to the NOS activity found in the smooth muscle. In ultrastructural studies of urothelial cells, NADPH-d reaction products were found predominantly on membranes of the nuclear envelope, endoplasmatic reticulum and mitochondria. In conclusion, NADPH-d staining of the urothelium cannot be taken as an indicator for the presence of constitutively expressed NOS. Activity of alkaline phosphatase and cytochrome P450 reductase may account for part of the NADPH-d reaction in urothelial cells. However, LPS treatment of rats caused expression of iNOS in urothelial cells.
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PMID:Morphological and biochemical investigation of nitric oxide synthase and related enzymes in the rat and pig urothelium. 1033 Apr 50

Shear stress causes release of nitric oxide (NO) from microvascular endothelial cells in vivo and stimulates their growth in vitro. After chronic electrical stimulation of lower hind limb skeletal muscles in the rat, measurements of capillary diameters and red blood cell velocity indicated that shear stress is increased in these vessels as a potential source of NO. This study therefore investigated whether NO is involved in capillary growth in stimulated muscles. Control rats or those stimulated for 2 or 7 days were treated with the NO synthase inhibitor, N(G)-nitro-l-arginine (l-NNA, 10 mg.day(-1) in drinking water), or water alone. After bromodeoxyuridine (BrdU) administration, extensor digitorum longus muscles were removed and frozen. Capillary supply was assessed in cryostat sections as capillary:fiber (C:F) ratio after staining for alkaline phosphatase; proliferation of capillary-linked and interstitial nuclei was evaluated by immunostaining for BrdU incorporation. C:F was not increased after 2 days of stimulation but the increase after 7 days (1.88 +/- 0.50 vs control 1.45 +/- 0.04, P < 0.001) was abolished by l-NNA (1.55 +/- 0.04, NS). The labeling index for BrdU-positive nuclei colocalized with capillaries as a percentage of total interstitial nuclei increased in muscles stimulated for 2 days (11.3 +/- 2.2%) and 7 days (10.6 +/- 0.8%) compared with controls (2.9 +/- 0.5%, P < 0.01) and was eliminated by l-NNA at both time points (3.1 +/- 0.6 and 1.0 +/- 0.6%, respectively; both P < 0.05 vs stimulated). A transient increase in BrdU labeling of interstitial nuclei not associated with capillaries (possibly fibroblasts) after 2 but not 7 days stimulation was eliminated by l-NNA treatment. These results suggest that NO is involved in capillary growth in chronically stimulated muscles possibly via its shear-stress-induced release from capillaries or from interstitial fibroblasts.
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PMID:Inhibition of capillary growth in chronically stimulated rat muscles by N(G)-nitro-l-arginine, nitric oxide synthase inhibitor. 1062 70

Oestradiol can stimulate osteoblast activity. Osteoblast function is thought to be regulated by nitric oxide (NO). We hypothesised that the effect of 17beta-oestradiol (17beta-E(2)) on osteoblast activity is mediated by NO. This hypothesis was tested using osteoblasts isolated from human trabecular bone, calvariae of rats, endothelial NO synthase (eNOS) gene-deficient mice, and their wild-type counterparts. Our results show that 17beta-E(2) dose-dependently stimulated proliferation and differentiation of primary human, rat and wild-typeosteoblasts. The presence of N(G)-monomethyl-l-arginine (10(-3) M), an inhibitor of NOS activity, blocked the 17beta-E(2)-(10(-7) M)-induced increases in thymidine incorporation (P < 0.01), alkaline phosphatase activity (P < 0.01) and bone nodule formation (P < 0.01) of wild-type, human and rat osteoblasts, respectively. Moreover, 17beta-E(2) did not induce a response in eNOS gene-deficient osteoblasts. 17beta-E(2) also increased total eNOS enzyme expression in rat osteoblasts. These findings indicate 17beta-E(2) modulates osteoblast function by NO-dependent mechanisms mediated via the eNOS isoform.
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PMID:Nitric oxide mediates 17beta-estradiol-stimulated human and rodent osteoblast proliferation and differentiation. 1106 1

Nitric oxide (NO) has been implicated in the local regulation of bone metabolism. However, the contribution made by specific NO synthase (NOS) enzymes is unclear. Here we show that endothelial NOS gene knockout mice (eNOS-/-) have marked abnormalities in bone formation. Histomorphometric analysis of eNOS-/- femurs showed bone volume and bone formation rate was reduced by up to 45% (P: < 0.01) and 52% (P: < 0.01), respectively. These abnormalities were prevalent in young (6 to 9 weeks old) adults but by 12 to 18 weeks bone phenotype was restored toward wild-type. Dual energy X-ray absorptiometry analysis confirmed the age-related bone abnormalities revealing significant reductions in femoral (P: < 0.05) and spinal bone mineral densities (P: < 0.01) at 8 weeks that were normalized at 12 weeks. Reduction in bone formation and volume was not related to increased osteoclast numbers or activity but rather to dysfunctional osteoblasts. Osteoblast numbers and mineralizing activity were reduced in eNOS-/- mice. In vitro, osteoblasts from calvarial explants showed retarded proliferation and differentiation (alkaline phosphatase activity and mineral deposition) that could be restored by exogenous administration of a NO donor. These cells were also unresponsive to 17ss-estradiol and had an attenuated chemotactic response to transforming growth factor-beta. In conclusion, eNOS is involved in the postnatal regulation of bone mass and lack of eNOS gene results in reduced bone formation and volume and this is related to impaired osteoblast function.
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PMID:Endothelial nitric oxide synthase gene-deficient mice demonstrate marked retardation in postnatal bone formation, reduced bone volume, and defects in osteoblast maturation and activity. 1114 98

Nitric oxide (NO) is a very small lipophilic molecule which rapidly diffuses and reaches the cytoplasmic components, and results in the activation of diverse biological function. It has been already reported that cultured osteoblasts synthesize NO in response to proinflammatory cytokines and lipopolysaccaride. In terms of the action of NO on bone metabolism, cytokine-induced NO by osteoblast inhibits bone resorption through inducing the apoptosis of osteoclast progenitor cells and suppressing the osteoclast activity. Also, NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine is reported to induce a dose-dependent inhibitory effect on the proliferation of osteoblast-like cell lines MG63 and ROS 17/2.8, which indicate that NO may stimulate cell proliferation. On the other hand, cytokine-induced NO is reported to reduce osteoblast activity significantly in high concentration, as was evidenced by inhibition of DNA synthesis, cell proliferation, alkaline phosphatase activity, and osteocalcin production. Thus, the effect of NO on osteoblast activities is still controversial. In the present study, S-nitroso-N-acetyl-dl-penicillamine(SNAP), NO donor enhanced DNA synthesis of MC3T3-E1 in vitro. This activation seems to be mediated by NO directly because specific NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO) partially attenuated the osteoblast proliferation induced by SNAP. On the other hand, the guanylate cyclase inhibitor, LY83583, failed to abolish the effect of SNAP on DNA synthesis of osteoblasts and 8-bromo cyclic guanosine 3',5'-monophosphate(cGMP), substituting for the accumulation of intracellular cGMP in osteoblasts, did not enhance the incorporation of 3H-thymidine(3H-TdR). It is, then, suggested that osteoblast proliferation might be enhanced by NO independently apart from the activation of cytoplasmic guanylate cyclase and cGMP-dependent mechanisms.
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PMID:Effect of nitric oxide on mouse clonal osteogenic cell, MC3T3-E1, proliferation in vitro. 1156 90

The purpose of this research was to investigate whether the effects of pulsed electromagnetic field (PEMF) stimulation on the osteoblast proliferation and differentiation are mediated by the increase in the nitric oxide (NO, nitrogen monoxide) synthesis. The osteoblasts (MC3T3-E1 cell line) were cultured in the absence (-NMMA group) or in the presence (+NMMA group) of the NO synthase inhibitor L-NMMA. First, osteoblasts were subjected to PEMF stimulation (15 Hz and 0.6 mT) up to 15 days. The DNA content and the NO concentration in the conditioned medium were determined on the 3rd, 7th, and 15th days of culture. Following, osteoblasts were stimulated in the proliferation (P-NMMA and P+NMMA groups) or in the differentiation (D-NMMA and D+NMMA groups) stages of maturation, and the alkaline phosphatase (AlPase) activity was determined on the 15th day of culture for all groups. PEMF stimulation increased significantly the nitrite concentration in the -NMMA group on the 3rd, 7th, and 15th days of culture. However, this effect was partially blocked in the +NMMA group. The DNA content in the -NMMA group, but not in the +NMMA group, increased significantly on the 3rd and 7th days of culture. The AlPase activity in the P-NMMA and D-NMMA groups, but not in the P+NMMA and D+NMMA groups, also increased significantly. In conclusion, the PEMF stimulatory effects on the osteoblasts proliferation and differentiation were mediated by the increase in the NO synthesis.
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PMID:Nitric oxide mediates the effects of pulsed electromagnetic field stimulation on the osteoblast proliferation and differentiation. 1217 15


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