ArticleThe Journal of physiology2009
PKC-permitted elevation of sarcolemmal KATP concentration may explain female-specific resistance to myocardial infarction.
Article in The Journal of physiology, 2009. 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, 26 citations in OpenAlex.
- Cardiac ventricular Kir6.1 ATP-sensitive potassium channels: an overlooked effector of cardioprotection.Frontiers in physiology · 2026Article
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- KArhiv za farmaciju · 2024Article
- A selective review of inhibitors of protein kinase C gamma: a neuroplasticity-related common pathway for psychiatric illness.Frontiers in drug delivery · 2024Review
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Isosteviol Sensitizes sarcKATP Channels towards Pinacidil and Potentiates Mitochondrial Uncoupling of Diazoxide in Guinea Pig Ventricular Myocytes.Oxidative medicine and cellular longevity · 2016Article
- ABCC9/SUR2 in the brain: Implications for hippocampal sclerosis of aging and a potential therapeutic target.Ageing research reviews · 2015Review
- Molecular Characterization of Reactive Oxygen Species in Myocardial Ischemia-Reperfusion Injury.BioMed research international · 2015Review
- Exercise and cardiac preconditioning against ischemia reperfusion injury.Current cardiology reviews · 2013Review
- Measuring and evaluating the role of ATP-sensitive K+ channels in cardiac muscle.Journal of molecular and cellular cardiology · 2012Review
- Sex differences in cardiomyocyte connexin43 expression.Journal of cardiovascular pharmacology · 2011Article
- Molecular mechanisms in exercise-induced cardioprotection.Cardiology research and practice · 2011Article
- Endosomal KATP channels as a reservoir after myocardial ischemia: a role for SUR2 subunits.American journal of physiology. Heart and circulatory physiology · 2011Article
- The ATP-sensitive K(+)-channel (K(ATP)) controls early left-right patterning in Xenopus and chick embryos.Developmental biology · 2010Article
- Femininity and sarcolemmal KATP channels: a matter of the heart and the heart of the matter.The Journal of physiology · 2009Article
- Life-long caloric restriction elicits pronounced protection of the aged myocardium: a role for AMPK.Mechanisms of ageing and developmentArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The female myocardium, relative to that of the male, exhibits sustained resistance to ischaemic tissue injury, a phenomenon termed sex-specific cardioprotection (SSC). SSC is dependent upon the sarcolemmal K(ATP) channel (sarcK(ATP)), and protein kinase C (PKC). Here we investigate whether PKC-mediated regulation of sarcK(ATP) concentration can explain this endogenous form of protection. Hearts from male (M) and female (F) rats were Langendorff-perfused for 30 min prior to either regional ischaemia-reperfusion (I/R), or global ischaemia (GISC). For both protocols, pre-ischaemic blockade of PKC was achieved by chelerythrine (Chel) in male (M + C) and female (F + C) hearts. Additional female hearts underwent sarcK(ATP) antagonism during I/R by HMR-1098 (HMR), either alone or in combination with Chel (HMR + Chel). GISC hearts were fractionated to assess cellular distribution of PKC and sarcK(ATP). Sex-specific infarct resistance was apparent under control I/R (F, 23 +/- 3% vs. M, 36 +/- 4%, P < 0.05) and abolished by Chel (F + C, 36 +/- 3%). Female infarct resistance was susceptible to sarcK(ATP) blockade (Control, 16 +/- 2% vs. HMR, 27 +/- 3%), and PKC blockade had no additional effect (HMR + Chel, 26 +/- 2%). The prevalence of Kir6.2 and SUR2 was higher in the sarcolemmal fractions of females (Kir6.2: F, 1.24 +/- 0.07 vs. M, 1.02 +/- 0.06; SUR2: F, 3.16 +/- 0.22 vs. M, 2.45 +/- 0.09; ratio units), but normalized by Chel (Kir6.2: F, 1.06 +/- 0.07 vs. M, 0.99 +/- 0.06; SUR2: F, 2.99 +/- 0.09 vs. M, 2.82 +/- 0.22, M; ratio units). Phosphorylation of sarcolemmal PKC was reduced by Chel (p-PKC/PKC: control, 0.43 +/- 0.02; Chel, 0.29 +/- 0.01; P < 0.01). We conclude that PKC-mediated regulation of sarcK(ATP) may account for the physiologically sustainable dependence of SSC upon both PKC and sarcK(ATP), and that this regulation involves PKC-permitted enrichment of the female sarcolemma with sarcK(ATP). As such, the PKC-sarcK(ATP) axis may represent a target for sustainable prophylactic induction of cardioprotection.
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Registered trials
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.