Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the role of elastin in arteries with respect to hypertension and hypertensive arterial disease, aortic elastin content and elastase-like enzyme activity were examined and compared in stroke-prone spontaneously hypertensive rats (SHRSP), which show malignant hypertension, and Wistar-Kyoto normotensive rats (WKY). The elastin content was lower, whereas the elastase-like activity was higher at 20 weeks of age in SHRSP than in WKY, so that the aortic elastin/enzyme ratio of SHRSP was lower than that in WKY. These differences were not found at 6 weeks of age (prehypertensive stage). For SHRSP anti-hypertensive treatment resulted in lowering the elastase-like activity and in increasing the elastin content in comparison to untreated animals. The subcellular distribution of the elastase-like activity closely correlated with that of 5'-nucleotidase activity, a plasma membrane marker enzyme. The results indicate involvement of a smooth muscle plasmalemmal elastase-like enzyme in vascular connective tissue metabolism in health and possibly also its participation in hypertensive arterial diseases.
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PMID:Elastin and elastase-like enzyme change in aorta of rat with malignant hypertension. 364 94

5'-Nucleotidase activity in the cerebrovascular system in stroke-prone spontaneously hypertensive rats was histochemically investigated. In the hypertensive rats, an enhancement of 5'-nucleotidase activity was observed already in the early stage of hypertension and the enzyme activity increased with advancing age. The enzyme activity appeared earlier and stronger in the larger arteries in the basal portion than the pial arteries in the convexity of the brain and arterioles in the brain parenchyma. The activity in the arterial walls proved to be particularly strong in the thickened parts showing cellular hyperplasia, mainly at the branching portions. The reaction products localized along the plasma membrane, and also in the cytoplasma in some parts where the activity was strong. Relationship between the increased 5'-nucleotidase activity and aging of the cells composing the cerebrovasculature resulted from an accelerated or repeated cell proliferation was discussed.
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PMID:Histochemical study on 5'-nucleotidase in the cerebrovascular system in stroke-prone spontaneously hypertensive rats. 627 95

1. Lipid peroxidation and membrane-related enzyme changes in the cerebral cortex of stroke-prone rats (SHRSP) and normotensive rats were examined at 5 and 20 weeks of age. 2. In vivo formation of thiobarbituric acid-reactant substances was higher in SHRSP at 20 weeks of age and in vitro generation of free malondialdehyde was greater in SHRSP brains, both at 5 and 20 weeks of age, as compared with those in WKY. 3. Membrane-associated enzymes such as Na/K-ATPase and 5'-nucleotidase activities were lower in 20-week-old SHRSP than in age-matched WKY. 4. These results indicate how very prone the SHRSP brain is toward lipid peroxidation and subsequent membrane-related enzyme changes.
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PMID:A comparative study on lipid peroxidation in cerebral cortex of stroke-prone spontaneously hypertensive and normotensive rats. 813 18

The pathological findings in 165 patients explored for malignant hyperthermia (MH) susceptibility are reported. The first group of 120 subjects were patients investigated for MH. These patients had suffered an attack of MH under anaesthetic or were members of families in which a subject had died of MH. In vitro contracture tests revealed 25 malignant hyperthermia susceptible (MHS) subjects, with positive contracture tests for halothane and caffeine, 5 malignant hyperthermia subjects with reaction to caffeine only (MHC), 3 malignant hyperthermia subjects with reaction to halothane only (MHH) and 87 malignant hyperthermia negative (MHN) subjects with normal contracture tests. The second group of 45 subjects had exertional heat stroke. In vitro contracture tests performed at least 3 months after the exertional heat stroke revealed 11 MHS, 6 MHC, 2 MHH subjects and 26 MHN. In both groups, whatever the in vitro contracture test results, pathological findings were heterogeneous and revealed various changes: rhabdomyolysis, mitochondrial myopathy, denervation, type II atrophy, AMPase deficiency, non-specific findings or normal features. Central core myopathy was only observed in the first subgroup and was the only disease significantly associated with MH. In contrast to previous reports, this study demonstrates the absence of a specific malignant hyperthermia or exertional heat stroke myopathy. Furthermore, the discovery of MHS subjects among the EHS group of patients highlights the need for systematic exploration of all these patients.
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PMID:Pathological findings in 165 patients explored for malignant hyperthermia susceptibility. 818 10

Adenosine, an endogenous neuroprotective agent, can be produced in the synaptic cleft from adenosine triphosphate (ATP) hydrolysis via the concerted action of two enzymes: ATP diphosphohydrolase and 5'-nucleotidase. The aim of the present study was to investigate such enzymatic activities in the hippocampus of rats subjected to single (2- or 10-minute) or double (2+10 minute, with a 24-hour interval in between, named preconditioned group) ischemic episodes. Ischemia was produced by four-vessel occlusion method. Histological analysis showed no cell death in 2-minute ischemia, and up to 90% of pyramidal CA(1) cell loss in the 10-minute ischemic group. As predicted, double ischemic rats displayed a significant cytoprotective effect (around 60%). Preconditioned rats presented a delayed enhancement in ATP diphosphohydrolase activity (for ATP and adenosine diphosphate hydrolysis) after 48 hours of reperfusion. 5'-nucleotidase activity was increased immediately after ischemic insult (for all groups) and after a late reperfusion period (48 hours). We suggest that preconditioning causes delayed changes in enzymatic activities that would conceivably lead to increased adenosine production. This effect could be related to cytoprotection seen in preconditioned rats.
J Stroke Cerebrovasc Dis
PMID:Nucleotide hydrolysis in rats submitted to global cerebral ischemia: a possible link between preconditioning and adenosine production. 1789 2

Ectoenzymes expressed on the surface of vascular cells and leukocytes modulate the ambient nucleotide milieu. CD73 is an ecto-5' nucleotidase that catalyzes the terminal phosphohydrolysis of AMP and resides in the brain on glial cells, cells of the choroid plexus, and leukocytes. Though CD73 tightens epithelial barriers, its role in the ischemic brain remains undefined. When subjected to photothrombotic arterial occlusion, CD73(-/-) mice exhibited significantly larger (49%) cerebral infarct volumes than wild-type mice, with concordant increases in local accumulation of leukocyte subsets (neutrophils, T lymphocytes, macrophages, and microglia). CD73(-/-) mice were rescued from ischemic neurologic injury by soluble 5'-nucleotidase. In situ, CD73(-/-) macrophages upregulated expression of costimulatory molecules far more than wild-type macrophages, with a sharp increase of the CD80/CD86 ratio. To define the CD73-bearing cells responsible for ischemic cerebroprotection, mice were subjected to irradiative myeloablation, marrow reconstitution, and then stroke following engraftment. Chimeric mice lacking CD73 in tissue had larger cerebral infarct volumes and more tissue leukosequestration than did mice lacking CD73 on circulating cells. These data show a cardinal role for CD73 in suppressing ischemic tissue leukosequestration. This underscores a critical role for CD73 as a modulator of brain inflammation and immune function.
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PMID:Tissue-resident ecto-5' nucleotidase (CD73) regulates leukocyte trafficking in the ischemic brain. 2229 Nov 83