ArticleAmerican journal of physiology. Heart and circulatory physiology2010
High-density lipoprotein determines adult mouse cardiomyocyte fate after hypoxia-reoxygenation through lipoprotein-associated sphingosine 1-phosphate.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 74 citations in OpenAlex.
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- High-Density Lipoprotein Signaling via Sphingosine-1-Phosphate Receptors Safeguards Spontaneously Hypertensive Rats against Myocardial Ischemia/Reperfusion Injury.Pharmaceutics · 2024Article
- Sphingolipid Mediators of Myocardial Pathology.Journal of lipid and atherosclerosis · 2020Review
- HDL protects against myocardial ischemia reperfusion injury via miR-34b and miR-337 expression which requires STAT3.PloS one · 2019Article
- Cardioprotective Effects of High-Density Lipoprotein Beyond its Anti-Atherogenic Action.Journal of atherosclerosis and thrombosis · 2018Review
- Analysis of Cell Signal Transduction Based on Kullback-Leibler Divergence: Channel Capacity and Conservation of Its Production Rate during Cascade.Entropy (Basel, Switzerland) · 2018Article
- The Conservation of Average Entropy Production Rate in a Model of Signal Transduction: Information Thermodynamics Based on the Fluctuation Theorem.Entropy (Basel, Switzerland) · 2018Article
- High-density lipoprotein protects cardiomyocytes against necrosis induced by oxygen and glucose deprivation through SR-B1, PI3K, and AKT1 and 2.The Biochemical journal · 2018Article
- Information Thermodynamics Derives the Entropy Current of Cell Signal Transduction as a Model of a Binary Coding System.Entropy (Basel, Switzerland) · 2018Article
- Sphingosine 1-Phosphate and Atherosclerosis.Journal of atherosclerosis and thrombosis · 2018Review
- Isolation of Plasma Lipoproteins as a Source of Extracellular RNA.Methods in molecular biology (Clifton, N.J.) · 2018Article
- High-density lipoprotein protects cardiomyocytes from oxidative stress via the PI3K/mTOR signaling pathway.FEBS open bio · 2017Article
- High-Density Lipoprotein Regulation of Mitochondrial Function.Advances in experimental medicine and biology · 2017Review
- High-density lipoprotein, mitochondrial dysfunction and cell survival mechanisms.Chemistry and physics of lipids · 2016Review
- Implication of sphingosin-1-phosphate in cardiovascular regulation.Frontiers in bioscience (Landmark edition) · 2016Review
- Speciated High-Density Lipoprotein Biogenesis and Functionality.Current atherosclerosis reports · 2016Review
- Sphingosine-1-phosphate reduces ischaemia-reperfusion injury by phosphorylating the gap junction protein Connexin43.Cardiovascular research · 2016Article
- Protective Effects of HDL Against Ischemia/Reperfusion Injury.Frontiers in pharmacology · 2016Review
- High-density lipoprotein inhibits mechanical stress-induced cardiomyocyte autophagy and cardiac hypertrophy through angiotensin II type 1 receptor-mediated PI3K/Akt pathway.Journal of cellular and molecular medicine · 2015Article
- Improving reconstituted HDL composition for efficient post-ischemic reduction of ischemia reperfusion injury.PloS one · 2015Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The lipid mediator sphingosine 1-phosphate (S1P) confers survival benefits in cardiomyocytes and isolated hearts subjected to oxidative stress. High-density lipoprotein (HDL) is a major carrier of S1P in the serum, but whether HDL-associated S1P directly mediates survival in a preparation composed exclusively of cardiomyocytes has not been demonstrated. Accordingly, we tested the hypothesis that signal activation and survival during simulated ischemia-reperfusion injury in response to HDL require lipoprotein-associated S1P. As a model, we used adult mouse cardiomyocytes subjected to hypoxia-reoxygenation. Cells were treated or not with autologous mouse HDL, which significantly increased myocyte viability as measured by trypan blue exclusion. This survival effect was abrogated by the S1P(1) and SIP(3) receptor antagonist VPC 23019. The selective S1P(3) antagonist CAY10444, the G(i) antagonist pertussis toxin, the MEK (MAPK/ERK) kinase inhibitor PD-98059, and the phosphoinositide-3 kinase inhibitor wortmannin also inhibited the prosurvival effect of HDL. We observed that HDL activated both Akt (protein kinase B) and the MEK1/2-ERK1/2 pathway and also stimulated phosphorylation of glycogen synthase kinase-3beta. ERK1/2 activation was through an S1P(1) subtype receptor-G(i) protein-dependent pathway, whereas the activation of Akt was inhibited by CAY10444, indicating mediation by S1P(3) subtype receptors. We conclude that HDL, via its cargo of S1P, can directly protect cardiomyocytes against simulated oxidative injury in the absence of vascular effects and that prosurvival signal activation is dependent on both S1P(1) and S1P(3) subtype receptors.
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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.