{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,29]],"date-time":"2025-10-29T03:40:17Z","timestamp":1761709217998,"version":"3.37.3"},"reference-count":45,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2016,6,1]]},"abstract":"<jats:p> Myocardial ischemia remains the primary cause of morbidity and mortality in the United States. Ischemic preconditioning (IPC) is a powerful form of endogenous protection against myocardial infarction. We studied alterations in K<jats:sub>ATP<\/jats:sub> channels surface density as a potential mechanism of the protection of IPC. Using cardiac-specific knockout of Kir6.2 subunits, we demonstrated an essential role for sarcolemmal K<jats:sub>ATP<\/jats:sub> channels in the infarct-limiting effect of IPC in the mouse heart. With biochemical membrane fractionation, we demonstrated that sarcolemmal K<jats:sub>ATP<\/jats:sub> channel subunits are distributed both to the sarcolemma and intracellular endosomal compartments. Global ischemia causes a loss of sarcolemmal K<jats:sub>ATP<\/jats:sub> channel subunit distribution and internalization to endosomal compartments. Ischemia-induced internalization of K<jats:sub>ATP<\/jats:sub> channels was prevented by CaMKII inhibition. K<jats:sub>ATP<\/jats:sub> channel subcellular redistribution was also observed with immunohistochemistry. Ischemic preconditioning before the index ischemia reduced not only the infarct size but also prevented K<jats:sub>ATP<\/jats:sub> channel internalization. Furthermore, not only did adenosine mimic IPC by preventing infarct size, but it also prevented ischemia-induced K<jats:sub>ATP<\/jats:sub> channel internalization via a PKC-mediated pathway. We show that preventing endocytosis with dynasore reduced both K<jats:sub>ATP<\/jats:sub> channel internalization and strongly mitigated infarct development. Our data demonstrate that plasticity of K<jats:sub>ATP<\/jats:sub> channel surface expression must be considered as a potentially important mechanism of the protective effects of IPC and adenosine. <\/jats:p>","DOI":"10.1152\/ajpheart.00158.2016","type":"journal-article","created":{"date-parts":[[2016,4,22]],"date-time":"2016-04-22T14:45:59Z","timestamp":1461336359000},"page":"H1558-H1566","source":"Crossref","is-referenced-by-count":23,"title":["Plasticity of sarcolemmal K<sub>ATP<\/sub> channel surface expression: relevance during ischemia and ischemic preconditioning"],"prefix":"10.1152","volume":"310","author":[{"given":"Hua-Qian","family":"Yang","sequence":"first","affiliation":[{"name":"Pediatrics,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monique N.","family":"Foster","sequence":"additional","affiliation":[{"name":"Pediatrics,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kundan","family":"Jana","sequence":"additional","affiliation":[{"name":"Pediatrics,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanne","family":"Ho","sequence":"additional","affiliation":[{"name":"Pediatrics,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael J.","family":"Rindler","sequence":"additional","affiliation":[{"name":"Cell Biology,"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1522-8326","authenticated-orcid":false,"given":"William A.","family":"Coetzee","sequence":"additional","affiliation":[{"name":"Pediatrics,"},{"name":"Physiology &amp; 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