{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T14:14:13Z","timestamp":1770819253673,"version":"3.50.1"},"reference-count":19,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>Type II secretory phospholipase A<jats:sub>2<\/jats:sub>(sPLA<jats:sub>2<\/jats:sub>) is a cardiovascular risk factor. We recently found depositions of sPLA<jats:sub>2<\/jats:sub>in the necrotic center of infarcted human myocardium and normally appearing cardiomyocytes adjacent to the border zone. The consequences of binding of sPLA<jats:sub>2<\/jats:sub>to ischemic cardiomyocytes are not known. To explore a potential effect of sPLA<jats:sub>2<\/jats:sub>on ischemic cardiomyocytes at a cellular level we used an in vitro model. The cardiomyocyte cell line H9c2 or adult cardiomyocytes were isolated from rabbits that were incubated with sPLA<jats:sub>2<\/jats:sub>in the presence of metabolic inhibitors to mimic ischemia-reperfusion conditions. Cell viability was established with the use of annexin V and propidium iodide or 7-aminoactinomycin D. Metabolic inhibition induced an increase of the number of flip-flopped cells, including a population that did not stain with propidium iodide and that was caspase-3 negative. sPLA<jats:sub>2<\/jats:sub>bound to the flip-flopped cells, including those negative for caspase-3. sPLA<jats:sub>2<\/jats:sub>binding induced cell death in these latter cells. In addition, sPLA<jats:sub>2<\/jats:sub>potentiated the binding of C-reactive protein (CRP) to these cells. We conclude that by binding to flip-flopped cardiomyocytes, including those that are caspase-3 negative and presumably reversibly injured, sPLA<jats:sub>2<\/jats:sub>may induce cell death and tag these cells with CRP.<\/jats:p>","DOI":"10.1152\/ajpheart.00887.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:13:37Z","timestamp":1425413617000},"page":"H2218-H2224","source":"Crossref","is-referenced-by-count":37,"title":["Type II secretory phospholipase A<sub>2<\/sub>binds to ischemic flip-flopped cardiomyocytes and subsequently induces cell death"],"prefix":"10.1152","volume":"285","author":[{"given":"R.","family":"Nijmeijer","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Willemsen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"C. J. L. 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M.","family":"Niessen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.12.6758"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.2001.280.6.H2572"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.5.11.1868978"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1016\/0165-6147(93)90071-Q"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/28.4.437"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.12.1280"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.100.1.96"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2760(96)00002-1"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1016\/S1388-1981(99)00157-2"},{"key":"REF10","doi-asserted-by":"crossref","unstructured":"Murakami M, Kudo I, and Inoue K.Molecular nature of phospholipases A2 involved in prostaglandin I2 synthesis in human umbilical vein endothelial cells. 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J Immunol157: 473\u2013479, 1996."},{"key":"REF18","doi-asserted-by":"crossref","unstructured":"Wolbink GJ, Schalkwijk C, Baars JW, Wagstaff J, van den Bosch H, and Hack CE.Therapy with interleukin-2 induces the systemic release of phospholipase-A2.Cancer Immunol Immunother41: 287\u2013292, 1995.","DOI":"10.1007\/BF01517216"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1001\/archsurg.133.11.1229"}],"container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajpheart.00887.2002","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,5,1]],"date-time":"2022-05-01T09:15:54Z","timestamp":1651396554000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajpheart.00887.2002"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003,11]]},"references-count":19,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2003,11]]}},"alternative-id":["10.1152\/ajpheart.00887.2002"],"URL":"https:\/\/doi.org\/10.1152\/ajpheart.00887.2002","relation":{},"ISSN":["0363-6135","1522-1539"],"issn-type":[{"value":"0363-6135","type":"print"},{"value":"1522-1539","type":"electronic"}],"subject":[],"published":{"date-parts":[[2003,11]]}}}