ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Plasticity of sarcolemmal KATP channel surface expression: relevance during ischemia and ischemic preconditioning.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
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- The cardioprotective role of sirtuins is mediated in part by regulating KAmerican journal of physiology. Cell physiology · 2023Article
- CL-705G: a novel chemical Kir6.2-specific KFrontiers in pharmacology · 2023Article
- Rab35 GTPase positively regulates endocytic recycling of cardiac KChannels (Austin, Tex.) · 2022Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- ROS‑associated mechanism of different concentrations of pinacidil postconditioning in the rat cardiac Nrf2‑ARE signaling pathway.Molecular medicine reports · 2021Article
- Atherogenic L5 LDL induces cardiomyocyte apoptosis and inhibits KLipids in health and disease · 2020Article
- Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020Review
- Myocardial death and dysfunction after ischemia-reperfusion injury require CaMKIIδ oxidation.Scientific reports · 2019Article
- Rab8a is involved in membrane trafficking of Kir6.2 in the MIN6 insulinoma cell line.Pflugers Archiv : European journal of physiology · 2019Article
- Mechanisms involved in adenosine pharmacological preconditioning-induced cardioprotection.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Review
- The trafficking protein, EHD2, positively regulates cardiac sarcolemmal KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Lipid signaling to membrane proteins: From second messengers to membrane domains and adapter-free endocytosis.The Journal of general physiology · 2018Review
- Ubiquitination mediates Kv1.3 endocytosis as a mechanism for protein kinase C-dependent modulation.Scientific reports · 2017Article
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
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6 authors at 1 institution in 1 country.
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Abstract
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 KATP 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 KATP channels in the infarct-limiting effect of IPC in the mouse heart. With biochemical membrane fractionation, we demonstrated that sarcolemmal KATP channel subunits are distributed both to the sarcolemma and intracellular endosomal compartments. Global ischemia causes a loss of sarcolemmal KATP channel subunit distribution and internalization to endosomal compartments. Ischemia-induced internalization of KATP channels was prevented by CaMKII inhibition. KATP channel subcellular redistribution was also observed with immunohistochemistry. Ischemic preconditioning before the index ischemia reduced not only the infarct size but also prevented KATP channel internalization. Furthermore, not only did adenosine mimic IPC by preventing infarct size, but it also prevented ischemia-induced KATP channel internalization via a PKC-mediated pathway. We show that preventing endocytosis with dynasore reduced both KATP channel internalization and strongly mitigated infarct development. Our data demonstrate that plasticity of KATP channel surface expression must be considered as a potentially important mechanism of the protective effects of IPC and adenosine.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.