Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phosphorylation of an M(r) 20,000 myosin light chain (MLC20) promotes the generation of contractile force through actin-myosin adenosine triphosphatase in most agonist-mediated vascular smooth muscle cell contraction. However, the role of calcium-mediated contractile processes in sustained arterial narrowing after subarachnoid hemorrhage remains unknown. In a femoral artery model of vasospasm, whole blood was applied to arteries in 54 rats for periods of 2 to 10 days; the contralateral artery treated with platelet-rich plasma served as matched control. During the early stage of vasospasm (Days 2-5), in the media of arteries exposed to blood, MLC20 phosphorylation (including diphosphorylated forms) increased significantly (30-38%; P < 0.05); total medial MLC20 during this interval was comparable to that in controls. After 5 days, however, total MLC20 decreased markedly (> 90%; P < 0.01) compared with controls; phosphorylated MLC20 was undetectable during this interval. MLC20-mediated contractile processes may be prominent in the early stages of arterial narrowing after subarachnoid hemorrhage; later stages are associated with the loss of MLC20 and the possible persistence of arterial narrowing by other mechanisms.
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PMID:The time course of myosin light-chain phosphorylation in blood-induced vasospasm. 764

Changes in Ca(++)-adenosine triphosphatase (ATPase) activity in the plasma membrane of smooth-muscle cells in the basilar arteries of dogs with experimental subarachnoid hemorrhage (SAH) were examined. The study methods included electron microscopic histochemistry and bioassay of the enzyme that exports cytoplasmic Ca++ to extracellular spaces. The Ca(++)-ATPase activity in the basilar artery increased significantly in response to the application of vasoconstrictive agents (prostaglandin F2 alpha and a phorbol ester), but decreased significantly 24 hours after experimental SAH, inversely with basilar artery contraction. Dogs that had undergone two arterial blood injections (double SAH) exhibited a further decrease in Ca(++)-ATPase activity as well as persistent contraction of the basilar artery for a longer period (at least 7 days) than was seen in animals with a single arterial blood injection. Bioassay of the enzyme also demonstrated a decrease in vascular Ca(++)-ATPase activity in dogs subjected to double SAH. These findings suggest that the early occurrence of and long-lasting decrease in Ca(++)-ATPase activity in dogs with experimental SAH induces a persistent disturbance of Ca++ homeostasis and indicates that damage to the plasma membrane in the cerebral arterial smooth-muscle cells proceeds to myonecrosis after SAH.
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PMID:Changes in Ca(++)-ATPase activity in smooth-muscle cell membranes of the canine basilar artery with experimental subarachnoid hemorrhage. 828 66

Patients with subarachnoid hemorrhage (SAH) who later suffer hydrocephalus show persistently high levels of transforming growth factor-beta 1 (TGF-beta 1) in the cerebrospinal fluid after the onset of SAH. Recombinant TGF-beta 1 induces hydrocephalus in mice. This study examined the spatial learning ability of rats after intraventricular administration of TGF-beta 1. Thirteen-week-old Wistar rats were treated with 0.8 or 8.0 micrograms of human recombinant TGF-beta 1 by direct injection or via osmotic pump. Three months later, their spatial learning ability was evaluated with a Morris water maze. Ventricular size, ultrastructural features, and sodium-potassium-adenosine triphosphatase (Na+, K(+)-ATPase) activity of the subarachnoid space were examined. All three TGF-beta 1-treated groups clearly exhibited impaired spatial learning ability, but they did not exhibit ventricular dilation. Histological examination revealed subarachnoid fibrosis and deactivation of Na+, K(+)-ATPase in the arachnoid cells. These findings are similar to those of our previous experiments involving injection of TGF-beta 1 in mice. The present and previous studies suggest that subarachnoid fibrosis is an important factor in the disturbance of the spatial learning ability of rats, whereas ventricular size is less important.
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PMID:Disturbed spatial learning of rats after intraventricular administration of transforming growth factor-beta 1. 1201 66