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dc.contributor.authorEthier, Michael F.
dc.contributor.authorYamaguchi, Hiroshi
dc.contributor.authorMadison, John M.
dc.date2022-08-11T08:09:32.000
dc.date.accessioned2022-08-23T16:34:54Z
dc.date.available2022-08-23T16:34:54Z
dc.date.issued2001-06-19
dc.date.submitted2008-01-24
dc.identifier.citation<p>Am J Physiol Lung Cell Mol Physiol. 2001 Jul;281(1):L126-33.</p>
dc.identifier.issn1040-0605 (Print)
dc.identifier.doi10.1152/ajplung.2001.281.1.L126
dc.identifier.pmid11404255
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38441
dc.description.abstractIn many cells, inhibition of sarcoplasmic reticulum (SR) Ca2+-ATPase activity induces a steady-state increase in cytosolic calcium concentration ([Ca2+]i) that is sustained by calcium influx. The goal was to characterize the response to inhibition of SR Ca2+-ATPase activity in bovine airway smooth muscle cells. Cells were dispersed from bovine trachealis and loaded with fura 2-AM (0.5 microM) for imaging of single cells. Cyclopiazonic acid (CPA; 5 microM) inhibited refilling of both caffeine- and carbachol-sensitive calcium stores. In the presence of extracellular calcium, CPA caused a transient increase in [Ca2+]i from 166 +/- 11 to 671 +/- 100 nM, and then [Ca2+]i decreased to a sustained level (CPA plateau; 236 +/- 19 nM) significantly above basal. The CPA plateau spontaneously declined toward basal levels after 10 min and was attenuated by discharging intracellular calcium stores. When CPA was applied during sustained stimulation with caffeine or carbachol, decreases in [Ca2+]i were observed. We concluded that the CPA plateau depended on the presence of SR calcium and that SR Ca2+-ATPase activity contributed to sustained increases in [Ca2+]i during stimulation with caffeine and, to a lesser extent, carbachol.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11404255&dopt=Abstract ">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1152/ajplung.2001.281.1.L126
dc.subjectAnimals
dc.subjectCaffeine
dc.subjectCalcium
dc.subjectCarbachol
dc.subjectCattle
dc.subjectCytosol
dc.subjectIndoles
dc.subjectIntracellular Membranes
dc.subjectMuscle, Smooth
dc.subjectOsmolar Concentration
dc.subjectTrachea
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEffects of cyclopiazonic acid on cytosolic calcium in bovine airway smooth muscle cells
dc.typeJournal Article
dc.source.journaltitleAmerican journal of physiology. Lung cellular and molecular physiology
dc.source.volume281
dc.source.issue1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/131
dc.identifier.contextkey417339
html.description.abstract<p>In many cells, inhibition of sarcoplasmic reticulum (SR) Ca2+-ATPase activity induces a steady-state increase in cytosolic calcium concentration ([Ca2+]i) that is sustained by calcium influx. The goal was to characterize the response to inhibition of SR Ca2+-ATPase activity in bovine airway smooth muscle cells. Cells were dispersed from bovine trachealis and loaded with fura 2-AM (0.5 microM) for imaging of single cells. Cyclopiazonic acid (CPA; 5 microM) inhibited refilling of both caffeine- and carbachol-sensitive calcium stores. In the presence of extracellular calcium, CPA caused a transient increase in [Ca2+]i from 166 +/- 11 to 671 +/- 100 nM, and then [Ca2+]i decreased to a sustained level (CPA plateau; 236 +/- 19 nM) significantly above basal. The CPA plateau spontaneously declined toward basal levels after 10 min and was attenuated by discharging intracellular calcium stores. When CPA was applied during sustained stimulation with caffeine or carbachol, decreases in [Ca2+]i were observed. We concluded that the CPA plateau depended on the presence of SR calcium and that SR Ca2+-ATPase activity contributed to sustained increases in [Ca2+]i during stimulation with caffeine and, to a lesser extent, carbachol.</p>
dc.identifier.submissionpathoapubs/131
dc.contributor.departmentDepartments of Medicine and Physiology
dc.source.pagesL126-33


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