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Abstract 17836: ATP Citrate Lyase Coordinates Lipid Synthesis and Expression Cell Cycle Regulating Genes to Promote Vascular Remodeling in Pulmonary Arterial Hypertension

2023· article· en· W4389944963 on OpenAlexaff
Charlotte Romanet, Yann Grobs, Sarah‐Eve Lemay, Alice Bourgeois, Tsukasa Shimauchi, Mabrouka Salem, Sandra Martineau, Sandra Breuils Bonnet, Mélanie Sauvaget, Charlie Théberge, François Potus, Steeve Provencher, Olivier Boucherat, Sébastien Bonnet

Bibliographic record

VenueCirculation · 2023
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicRNA modifications and cancer
Canadian institutionsMinistère de l’Emploi et de la Solidarité Sociale (Québec)Hôpital Saint-François d'AssiseInstitut universitaire de cardiologie et de pneumologie de Québec
Fundersnot available
KeywordsATP citrate lyaseP300-CBP Transcription FactorsCell growthCancer researchHistone H3GlycolysisBiologyAnaerobic glycolysisCell biologyHistoneBiochemistryCitrate synthaseHistone AcetyltransferasesEnzymeGene

Abstract

fetched live from OpenAlex

INTRODUCTION: Pulmonary arterial hypertension (PAH) is characterized by progressive obliteration of distal pulmonary arteries (PAs) due to enhanced proliferation, suppressed apoptosis and increased migration of PA smooth muscle cells (PASMCs). Like cancer cells, this abnormal phenotype of PASMCs is driven by epigenetic reprogramming and fueled by a metabolic shift towards glycolysis. ATP-Citrate Lyase (ACLY) is a nuclear-cytosolic enzyme that converts citrate to acetyl-CoA, which serves as substrate for histone acetyltransferases regulating gene expression and as a building block for lipid synthesis (required for proliferating cells to generate membrane). ACLY has recently emerged as a key player and therapeutic target in cancer. However, its role in PAH is unknown. METHODS/RESULTS: ACLY, p-ACLY (active form) expression and its nuclear localization were increased in distal PAs and PASMCs from PAH patients (WB and IF, p<0.01). Similar results were observed in the Sugen/Hypoxia (Su/Hx) animal models. In vitro , ACLY inhibition (BMS, siRNA) decreases PAH-PASMCs proliferation (PLK1; Ki67; p<0,01) and survival (Survivin; Annexin-V; p<0.01). These effects were accompanied with a decreased glycolysis (PFKBP3, p-PDH) and increased OCR/ECAR (Seahorse). Moreover, ACLY inhibition decreases the PAH-PASMCs migratory potential. Using RNA-Seq, we demonstrated that inhibition of ACLY downregulates genes associated with cell division and lipid synthesis. Further experiments revealed that ACLY promotes nuclear acetyl-CoA production favoring acetylation of H3K27, H3K9, H4, and GCN5-mediated transcriptional activation of genes responsible for cell cycle progression. Accordingly, we demonstrated that GCN5 inhibition decreases proliferation and survival of PAH-PASMCs (Ki67, AnnexinV). In vivo , Acly loss-of-function targeted to SMCs conferred protection against Su/HX-induced PAH in mice (echo and RHC). Accordingly, pharmacological inhibition of ACLY using BMS-303141 or Bempedoic Acid improved hemodynamics (RVSP, mPAP, SV, TPR, p<0.05) and vascular remodeling (EVG, p<0.05) in Su/Hx rats with established PAH. CONCLUSION: We demonstrated that ACLY inhibition may represent a novel therapeutic avenue to improve vascular remodeling in PAH.

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 score0.011
Threshold uncertainty score0.037

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)0.0110.002

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 head0.234
Teacher spread0.216 · 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".

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Citations0
Published2023
Admission routes1
Has abstractyes

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