{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T17:46:55Z","timestamp":1760204815805},"reference-count":0,"publisher":"Portland Press Ltd.","issue":"3","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1991,8,1]]},"abstract":"<jats:p>Previous studies have concluded that cytosolic Ca2+ [(Ca2+]i) transients are essential for neutrophils (PMN) to degranulate and make superoxide anion when challenged with the receptor agonists N-formyl-methionyl-leucyl-phenylalanine, platelet-activating factor and leukotriene B4. This view is based on the profound unresponsiveness of PMN that have their [Ca2+]i fixed at resting levels by removing storage Ca2+ and loading the cells with greater than or equal to 20 microM of a Ca2+ chelator, quin2 AM. We too observed this unresponsive state in PMN loaded with 10-32 microM-quin2 AM, fura-2 AM or 1,2-bis-(2-aminophenoxy) ethane-NNN'N'-tetra-acetic acid (BAPTA). When loaded with less than or equal to 1 microM fura-2 AM, however, Ca(2+)-depleted PMN failed to alter [Ca2+]i appreciably, yet still had substantial degranulation and superoxide-anion-generating responses to the receptor agonists. Function thus did not require [Ca2+]i transients. Moreover, Ca(2+)-depleted PMN had 20-35% decreases in receptor numbers for each of the three agonists, and chelator loading of these cells decreased receptor availability by 30-50%. All receptor losses were reversed by incubating PMN with Ca2+ at 37 degrees C, but not at 4 degrees C, and agonist binding at 4 degrees C was not influenced by the presence or absence of extracellular Ca2+. Ca2+ thus caused PMN to up-regulate their agonist receptors at 37 degrees C, and the effect persisted at 4 degrees C regardless of ambient Ca2+. We conclude that Ca2+ acts in at least three ways to regulate responses to receptor agonists. First, some pool of (probably cellular) Ca2+ maintains receptor expression. Second, [Ca2+]i transients potentiate, but are not required for, function. The [Ca2+]i pool may or may not be the same as that influencing receptors. Finally, another pool(s) of Ca2+ signals or permits responses. This last pool, rather than [Ca2+]i transients, appears essential for the bioactions of standard Ca(2+)-mobilizing stimuli.<\/jats:p>","DOI":"10.1042\/bj2770705","type":"journal-article","created":{"date-parts":[[2015,8,10]],"date-time":"2015-08-10T21:22:29Z","timestamp":1439241749000},"page":"705-711","update-policy":"http:\/\/dx.doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Roles of Ca2+ in human neutrophil responses to receptor agonists"],"prefix":"10.1042","volume":"277","author":[{"given":"J T","family":"O'Flaherty","sequence":"first","affiliation":[{"name":"Wake Forest University Medical Center, Department of Medicine, Section on Infectious Diseases, Winston-Salem, NC 27103, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A G","family":"Rossi","sequence":"additional","affiliation":[{"name":"Wake Forest University Medical Center, Department of Medicine, Section on Infectious Diseases, Winston-Salem, NC 27103, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D P","family":"Jacobson","sequence":"additional","affiliation":[{"name":"Wake Forest University Medical Center, Department of Medicine, Section on Infectious Diseases, Winston-Salem, NC 27103, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J F","family":"Redman","sequence":"additional","affiliation":[{"name":"Wake Forest University Medical Center, Department of Medicine, Section on Infectious Diseases, Winston-Salem, NC 27103, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","container-title":["Biochemical Journal"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/portlandpress.com\/biochemj\/article-pdf\/277\/3\/705\/604422\/bj2770705.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/portlandpress.com\/biochemj\/article-pdf\/277\/3\/705\/604422\/bj2770705.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,11,23]],"date-time":"2021-11-23T22:02:00Z","timestamp":1637704920000},"score":1,"resource":{"primary":{"URL":"https:\/\/portlandpress.com\/biochemj\/article\/277\/3\/705\/28392\/Roles-of-Ca2-in-human-neutrophil-responses-to"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1991,8,1]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1991,8,1]]}},"URL":"https:\/\/doi.org\/10.1042\/bj2770705","relation":{},"ISSN":["0264-6021","1470-8728"],"issn-type":[{"value":"0264-6021","type":"print"},{"value":"1470-8728","type":"electronic"}],"subject":[],"published":{"date-parts":[[1991,8,1]]}}}