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Record W2764240839 · doi:10.1093/eurheartj/ehx494.4805

4805GLP-1(28–36) prevents ischemic cardiac injury by modulating metabolism and activating soluble adenylyl cyclase in coronary vascular cells

2017· article· en· W2764240839 on OpenAlexaff
M. Ahsan Siraj, Dhanwantee Mundil, Talat Afroze, Michael B. Wheeler, G. Keller, Mansoor Husain

Bibliographic record

VenueEuropean Heart Journal · 2017
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicEicosanoids and Hypertension Pharmacology
Canadian institutionsUniversity of TorontoUniversity Health Network
Fundersnot available
KeywordsMedicineAdenylyl cyclaseCardiologyInternal medicineIschemic injuryMetabolismPharmacologyIschemiaReceptor

Abstract

fetched live from OpenAlex

Background: Cardiovascular disease (CVD) is increasingly attributable to type-2 diabetes (T2D) and obesity, with the incidence of T2D predicted to double by 2030. However, mechanisms underlying the pathophysiology of CVD in T2D are poorly understood. Pre-clinical studies in animals and recent human clinical trials have demonstrated robust cardioprotective actions of incretin glucagon-like peptide-1 (GLP-1), related peptides and drugs. How GLP-1 prevents acute myocardial ischemia-reperfusion injury (IRI) as well as chronic myocardial ischemic injury has not been established. We previously described that GLP-1(28–36), a small metabolite of GLP-1, is as protective as the parent peptide in ex vivo isolated heart IRI and in vivo experimental myocardial infarction (MI) models in mice, and that these effects require soluble adenylyl cyclase (sAC), but not the known GLP-1 receptor. Here we define the molecular mechanisms and cell types in which GLP-1(28–36) activates sAC. Methods and results: Immunoblots reveal that mouse and human coronary artery smooth muscle cells (caSMC) and human coronary artery endothelial cells (caEC) express sAC, while mouse neonatal ventricular cardiomyocytes (CM), a mouse atrial CM cell line (HL-1), and human embryonic stem cell (ESC)-derived CM do not. Using pharmacological inhibitors of sAC, sAC-null mice and siRNA against sAC, we demonstrate that GLP-1(28–36) causes sAC-dependent increases in cAMP, activation of PKA, and cytoprotection from oxidative stress injury in both mouse and human caSMC. Moreover, GLP-1(28–36) increases cAMP responses in human caEC and probenecid, which blocks the anion (HCO3) entry required for sAC activity, abrogates these effects. By contrast, human ESC-derived CM shows no cAMP or cytoprotection responses to GLP-1(28–36). Next, we show in caSMC that GLP-1(28–36) causes dose-dependent increases in intracellular ATP, a known substrate of sAC. Affinity pull-down experiments using biotinylated-GLP-1(28–36), proteomic analysis with mass spectrometry, and confirmatory immunoblots suggest that GLP-1(28–36) interacts with mitochondrial trifunctional protein alpha (MTPα), an enzyme involved in fatty acid metabolism, and does not directly interact with sAC. Using extracellular flux analysis of caSMC and caEC, and siRNA against MTPα, we demonstrate that the ability of GLP-1(28–36) to shift substrate utilization towards the energy efficient glucose utilization and away from the high energy consuming fatty acid oxidation is dependent on MTPα.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.018
GPT teacher head0.285
Teacher spread0.267 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2017
Admission routes1
Has abstractyes

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