{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,3]],"date-time":"2025-12-03T17:45:30Z","timestamp":1764783930900},"reference-count":38,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,2,16]],"date-time":"2017-02-16T00:00:00Z","timestamp":1487203200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Fundamemntal Clinical Pharma"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We reported that coronary spasm was induced in the transgenic mice with the increased phospholipase C (<jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>)\u2010\u03b41 activity. We investigated the effect of enhanced <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\u2010\u03b41 on Ca<jats:sup>2+<\/jats:sup> influx and its underlying mechanisms. We used human embryonic kidney (<jats:styled-content style=\"fixed-case\">HEK<\/jats:styled-content>)\u2010293 and coronary arteries smooth muscle cells (<jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>). Intracellular free Ca<jats:sup>2+<\/jats:sup> concentration ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>; n<jats:sc>m<\/jats:sc>) was measured by fura\u20102, and Ca<jats:sup>2+<\/jats:sup> influx was evaluated by the increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> after addition of extracellular Ca<jats:sup>2+<\/jats:sup>. Acetylcholine (<jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h) was used to induce Ca<jats:sup>2+<\/jats:sup> influx. <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h\u2010induced peak Ca<jats:sup>2+<\/jats:sup> influx was 19 \u00b1 3 in control <jats:styled-content style=\"fixed-case\">HEK<\/jats:styled-content>\u2010293 cells and 71 \u00b1 8 in the cells with <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\u2010\u03b41 overexpression (<jats:italic>P<\/jats:italic> &lt; 0.05 between two groups). Nifedipine partially suppressed this Ca<jats:sup>2+<\/jats:sup> influx, whereas either 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content> or knockdown of classical transient receptor potential channel 6 (<jats:styled-content style=\"fixed-case\">TRPC<\/jats:styled-content>6) blocked this Ca<jats:sup>2+<\/jats:sup> influx. In the human <jats:styled-content style=\"fixed-case\">CASMC<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> AC<\/jats:styled-content>h\u2010induced peak Ca<jats:sup>2+<\/jats:sup> influx was 29 \u00b1 6 in the control and was increased to 45 \u00b1 16 by <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\u2010\u03b41 overexpression (<jats:italic>P<\/jats:italic> &lt; 0.05). Like <jats:styled-content style=\"fixed-case\">HEK<\/jats:styled-content>\u2010293 cells, pretreatment with nifedipine partially suppressed Ca<jats:sup>2+<\/jats:sup> influx, whereas either 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content> or knockdown of <jats:styled-content style=\"fixed-case\">TRPC<\/jats:styled-content>6 blocked it. <jats:styled-content style=\"fixed-case\">AC<\/jats:styled-content>h\u2010induced Ca<jats:sup>2+<\/jats:sup> influx was enhanced by <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\u2010\u03b41 overexpression, and was blocked partially by nifedipine and completely by 2\u2010<jats:styled-content style=\"fixed-case\">APB<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">TRPC<\/jats:styled-content>\u2010mediated Ca<jats:sup>2+<\/jats:sup> influx may be related to the enhanced Ca<jats:sup>2+<\/jats:sup> influx in <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\u2010\u03b41 overexpression.<\/jats:p>","DOI":"10.1111\/fcp.12269","type":"journal-article","created":{"date-parts":[[2017,1,20]],"date-time":"2017-01-20T22:16:43Z","timestamp":1484950603000},"page":"383-391","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Enhanced transient receptor potential channel\u2010mediated Ca<sup>2+<\/sup> influx in the cells with phospholipase C\u2010\u03b41 overexpression: its possible role in coronary artery spasm"],"prefix":"10.1111","volume":"31","author":[{"given":"Kazuo","family":"Murakami","sequence":"first","affiliation":[{"name":"Department of Cardiology Hirosaki University Graduate School of Medicine 5 Zaifu\u2010cho Hirosaki Hirosaki Aomori Prefecture Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomohiro","family":"Osanai","sequence":"additional","affiliation":[{"name":"Department of Nursing Hirosaki University Graduate School of Health Science 66\u20101 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